General Information of the Molecule (ID: Mol01262)
Name
Growth arrest specific 5 (GAS5) ,Homo sapiens
Synonyms
GAS5
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Molecule Type
LncRNA
Gene Name
HANR
Gene ID
60674
Location
chr1:173858559-173868882[-]
Ensembl ID
ENSG00000234741
HGNC ID
HGNC:16355
        Click to Show/Hide the Complete Species Lineage
Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  EADR: Epigenetic Alteration of DNA, RNA or Protein
  RTDM: Regulation by the Disease Microenvironment
Drug Resistance Data Categorized by Drug
Approved Drug(s)
11 drug(s) in total
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Cisplatin
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Cervical cancer [1]
Resistant Disease Cervical cancer [ICD-11: 2C77.0]
Resistant Drug Cisplatin
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
Cell invasion Activation hsa05200
Cell migration Activation hsa04670
STAT3 signaling pathway Activation hsa04550
In Vitro Model Hela cells Cervix uteri Homo sapiens (Human) CVCL_0030
Siha cells Cervix uteri Homo sapiens (Human) CVCL_0032
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay; Flow cytometry assay; Colony formation assay
Mechanism Description Down-regulation of LncRNA GAS5 strengthen cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21.
Disease Class: Non-small cell lung cancer [2]
Resistant Disease Non-small cell lung cancer [ICD-11: 2C25.Y]
Resistant Drug Cisplatin
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation miR21/PTEN signaling pathway Regulation hsa05206
In Vitro Model A549 cells Lung Homo sapiens (Human) CVCL_0023
H460 cells Lung Homo sapiens (Human) CVCL_0459
H1299 cells Lung Homo sapiens (Human) CVCL_0060
Sk-MES-1 cells Lung Homo sapiens (Human) CVCL_0630
NCI-H358 cells Lung Homo sapiens (Human) CVCL_1559
16HBE cells Lung Homo sapiens (Human) CVCL_0112
H157 cells Lung Homo sapiens (Human) CVCL_2458
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
MTT assay; Soft agar assay
Mechanism Description GAS5 could compete with PTEN for miR21 binding, GAS5 downregulation can induce trastuzumab resistance of breast cancer.
Disease Class: Non-small cell lung cancer [2]
Resistant Disease Non-small cell lung cancer [ICD-11: 2C25.Y]
Resistant Drug Cisplatin
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation AKT signaling pathway Regulation hsa04151
In Vitro Model A549 cells Lung Homo sapiens (Human) CVCL_0023
H460 cells Lung Homo sapiens (Human) CVCL_0459
H1299 cells Lung Homo sapiens (Human) CVCL_0060
Sk-MES-1 cells Lung Homo sapiens (Human) CVCL_0630
NCI-H358 cells Lung Homo sapiens (Human) CVCL_1559
16HBE cells Lung Homo sapiens (Human) CVCL_0112
H157 cells Lung Homo sapiens (Human) CVCL_2458
Experiment for
Molecule Alteration
qPCR
Experiment for
Drug Resistance
MTT assay; Soft agar assay
Mechanism Description GAS5 could compete with PTEN for miR21 binding, GAS5 downregulation can induce trastuzumab resistance of breast cancer By negatively regulating the intracellular levels of PI3k, PTEN exerts a suppressive effect on tumor through AkT pathway. GAS5 regulated NSCLC chemo-sensitivity to DDP-based therapy through PTEN pathway.
Disease Class: Cervical cancer [3]
Resistant Disease Cervical cancer [ICD-11: 2C77.0]
Resistant Drug Cisplatin
Molecule Alteration Expression
Down-regulation
Experimental Note Identified from the Human Clinical Data
Cell Pathway Regulation PI3K/AKT signaling pathway Activation hsa04151
In Vitro Model Hela cells Cervix uteri Homo sapiens (Human) CVCL_0030
Siha cells Cervix uteri Homo sapiens (Human) CVCL_0032
Caski cells Uterus Homo sapiens (Human) CVCL_1100
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
CCK8 assay
Mechanism Description The low level of GAS5 can down-regulate PTEN by interacting with miR21 because PTEN is one of the genes in the PI3k/Akt/mTOR pathway that can be regulated by GAS5 negatively. The low expression of PTEN activates the PI3k/Akt pathway.
Disease Class: Non-small cell lung cancer [4]
Resistant Disease Non-small cell lung cancer [ICD-11: 2C25.Y]
Resistant Drug Cisplatin
Molecule Alteration Expression
Down-regulation
Experimental Note Identified from the Human Clinical Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
In Vitro Model A549 cells Lung Homo sapiens (Human) CVCL_0023
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay
Mechanism Description GAS5 downregulation is associated with cisplatin resistance in NSCLC. GAS5 can inhibit autophagy and therefore enhance cisplatin sensitivity in NSCLC cells.
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Epithelial ovarian cancer [5]
Sensitive Disease Epithelial ovarian cancer [ICD-11: 2B5D.0]
Sensitive Drug Cisplatin
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
Cell formation Inhibition hsa05200
Cell invasion Inhibition hsa05200
MAPK signaling pathway Regulation hsa04010
In Vitro Model HEY cells Ovary Homo sapiens (Human) CVCL_0297
SkOV3 cells Ovary Homo sapiens (Human) CVCL_0532
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
RT-qPCR
Experiment for
Drug Resistance
CCK8 assay; Flow cytometry assay
Mechanism Description GAS5 might regulate PARP1 expression by recruiting the transcription factor E2F4 to its promoter, and then affect the MAPk pathway activity and enhance sensitivity to DDP of OC both in vitro and in vivo.
Docetaxel
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [6]
Resistant Disease Prostate cancer [ICD-11: 2C82.0]
Resistant Drug Docetaxel
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
In Vitro Model PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Fluorescence microscopy test apoptosis assay
Mechanism Description Transient expression of GAS5 enhances apoptosis and decreases the survival of 22Rv1 cells, forced variation of GAS5 gene expression can modulate cellular responses to various apoptotic stimuli, including a range of chemotherapeutic drugs.
Doxorubicin
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Bladder urothelial carcinoma [7]
Resistant Disease Bladder urothelial carcinoma [ICD-11: 2C94.2]
Resistant Drug Doxorubicin
Molecule Alteration Expression
Up-regulation
Experimental Note Identified from the Human Clinical Data
In Vitro Model J82 cells Bladder Homo sapiens (Human) CVCL_0359
T24 cells Bladder Homo sapiens (Human) CVCL_0554
T24/DOX cells Bladder Homo sapiens (Human) CVCL_0554
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay; Dual-color flow cytometric method; Annexin V-FITC apoptosis assay
Mechanism Description Long noncoding RNA GAS5 inhibits malignant proliferation and chemotherapy resistance to doxorubicin in bladder transitional cell carcinoma.
Everolimus
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [8]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug Everolimus
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell proliferation Inhibition hsa05200
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
PNT2C2 cells Prostate Homo sapiens (Human) CVCL_4889
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
GAS5 assay; MTS assay
Mechanism Description First generation mTORC1, combined mTORC1/mTORC2 and dual PI3k/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 LncRNA sensitized PC-3 and DU 145 cells to these agents.
Fluorouracil
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Pancreatic cancer [9]
Resistant Disease Pancreatic cancer [ICD-11: 2C10.3]
Resistant Drug Fluorouracil
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Hippo signaling pathway Inhibition hsa04390
In Vitro Model SW1990 cells Pancreas Homo sapiens (Human) CVCL_1723
5-FU cells Colon Homo sapiens (Human) CVCL_1846
PATU8988 Pancreas Homo sapiens (Human) CVCL_1847
PATU8988 cells Pancreas Homo sapiens (Human) CVCL_1846
SW1990/GEM cells Pancreas Homo sapiens (Human) CVCL_ZW98
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay
Mechanism Description GAS5 regualtes Hippo signaling pathway via miR181c-5p to antagonize the development of multidrug resistance in pancreatic cancer cells. GAS5 regulated chemoresistance and Hippo pathway of pancreatic cancer cells via miR181c-5p/Hippo.
Gefitinib
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Lung adenocarcinoma [10]
Sensitive Disease Lung adenocarcinoma [ICD-11: 2C25.0]
Sensitive Drug Gefitinib
Molecule Alteration Expression
Up-regulation
Experimental Note Identified from the Human Clinical Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
Cell invasion Inhibition hsa05200
Cell migration Inhibition hsa04670
Cell proliferation Inhibition hsa05200
EGFR signaling pathway Inhibition hsa01521
In Vitro Model H1975 cells Lung Homo sapiens (Human) CVCL_1511
A549 cells Lung Homo sapiens (Human) CVCL_0023
H1299 cells Lung Homo sapiens (Human) CVCL_0060
HCC827 cells Lung Homo sapiens (Human) CVCL_2063
16HBE cells Lung Homo sapiens (Human) CVCL_0112
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay; EdU assay
Mechanism Description GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. Furthermore, lower GAS5 expression levels were associated with larger tumor sizes, poor tumor differentiation, and advanced pathological stages. However, GAS5 was almost equally expressed between benign tumors compared with the adjacent normal tissues. GAS5 was also overexpressed in EGFR-TkI sensitive cell lines compared with the resistant cell line. Using MTT, EdU incorporation, and colony formation assays, we showed that GAS5-expressing A549 cells displayed an elevated level of cell death. In addition to its pro-apoptotic effect in the A549 cell line, GAS5 overexpression also suppressed the growth of A549-derived tumors in nude mice treated with gefitinib. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins.
Gemcitabine
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Regulation by the Disease Microenvironment (RTDM) Click to Show/Hide
Disease Class: Pancreatic cancer [11]
Sensitive Disease Pancreatic cancer [ICD-11: 2C10.3]
Sensitive Drug Gemcitabine
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell invasion Inhibition hsa05200
Cell migration Inhibition hsa04670
Cell proliferation Inhibition hsa05200
miR221/SOCS3 signaling pathway Regulation hsa05206
In Vitro Model BxPC-3 cells Pancreas Homo sapiens (Human) CVCL_0186
PANC-1 cells Pancreas Homo sapiens (Human) CVCL_0480
Capan-2 cells Pancreas Homo sapiens (Human) CVCL_0026
AsPC-1 cells Pancreas Homo sapiens (Human) CVCL_0152
SW1990 cells Pancreas Homo sapiens (Human) CVCL_1723
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
Western blot analysis; RT-qPCR
Experiment for
Drug Resistance
CCK8 assay; Flow cytometry assay
Mechanism Description Overexpression of GAS5 inhibits proliferation, migration, and chemotherapy resistance by suppressing the emt and tumor stem cell-like properties. LncRNA GAS5 functioned as a competing endogenous RNA for miR-221, and it suppressed cell growth, metastasis, and gemcitabine resistance in PC by regulating the miR-221/SOCS3 pathway mediating EMT and tumor stem cell self-renewal.
Mitoxantrone
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [6]
Resistant Disease Prostate cancer [ICD-11: 2C82.0]
Resistant Drug Mitoxantrone
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
In Vitro Model PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Fluorescence microscopy test apoptosis assay
Mechanism Description Transient expression of GAS5 enhances apoptosis and decreases the survival of 22Rv1 cells, forced variation of GAS5 gene expression can modulate cellular responses to various apoptotic stimuli, including a range of chemotherapeutic drugs.
Sirolimus
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Mantle cell lymphoma [12]
Resistant Disease Mantle cell lymphoma [ICD-11: 2A85.0]
Resistant Drug Sirolimus
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
Cell proliferation Activation hsa05200
mTOR signaling pathway Regulation hsa04150
In Vitro Model Z138 cells Peripheral blood Homo sapiens (Human) CVCL_B077
Jeko-1 cells Blood Homo sapiens (Human) CVCL_1865
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Nigrosin exclusion analysis
Mechanism Description Small interfering RNAs (sirRNAs) targeting GAS5 protect the cell viability and proliferation of jeko-1 and z-138 cells from the inhibitory effects of mTOR inhibitors result in rapamycin resistance.
Disease Class: Mantle cell lymphoma [12]
Resistant Disease Mantle cell lymphoma [ICD-11: 2A85.0]
Resistant Drug Sirolimus
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
Cell proliferation Activation hsa05200
mTOR signaling pathway Regulation hsa04150
In Vitro Model Z138 cells Peripheral blood Homo sapiens (Human) CVCL_B077
Jeko-1 cells Blood Homo sapiens (Human) CVCL_1865
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Nigrosin exclusion analysis
Mechanism Description Small interfering RNAs (sirRNAs) targeting GAS5 protect the cell viability and proliferation of jeko-1 and z-138 cells from the inhibitory effects of mTOR inhibitors result in rapamycin resistance.
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [8]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug Sirolimus
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell proliferation Inhibition hsa05200
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
PNT2C2 cells Prostate Homo sapiens (Human) CVCL_4889
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
GAS5 assay; MTS assay
Mechanism Description First generation mTORC1, combined mTORC1/mTORC2 and dual PI3k/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 LncRNA sensitized PC-3 and DU 145 cells to these agents.
Temsirolimus
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Mantle cell lymphoma [12]
Resistant Disease Mantle cell lymphoma [ICD-11: 2A85.0]
Resistant Drug Temsirolimus
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
Cell proliferation Activation hsa05200
mTOR signaling pathway Regulation hsa04150
In Vitro Model Z138 cells Peripheral blood Homo sapiens (Human) CVCL_B077
Jeko-1 cells Blood Homo sapiens (Human) CVCL_1865
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Nigrosin exclusion analysis
Mechanism Description Small interfering RNAs (sirRNAs) targeting GAS5 protect the cell viability and proliferation of jeko-1 and z-138 cells from the inhibitory effects of mTOR inhibitors result in rapamycin resistance.
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [8]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug Temsirolimus
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell proliferation Inhibition hsa05200
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
PNT2C2 cells Prostate Homo sapiens (Human) CVCL_4889
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
GAS5 assay; MTS assay
Mechanism Description First generation mTORC1, combined mTORC1/mTORC2 and dual PI3k/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 LncRNA sensitized PC-3 and DU 145 cells to these agents.
Trastuzumab
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: HER2 positive breast cancer [13]
Resistant Disease HER2 positive breast cancer [ICD-11: 2C60.8]
Resistant Drug Trastuzumab
Molecule Alteration Expression
Down-regulation
Experimental Note Identified from the Human Clinical Data
Cell Pathway Regulation Cell proliferation Activation hsa05200
mTOR signaling pathway Activation hsa04150
In Vitro Model SkBR3 cells Breast Homo sapiens (Human) CVCL_0033
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay
Mechanism Description Down-regulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer.Expression of the LncRNA GAS5 was decreased in trastuzumab-resistant SkBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. This work identifies GAS5 as a novel prognostic marker and candidate drug target for HER2-positive breast cancer.
Clinical Trial Drug(s)
2 drug(s) in total
Click to Show/Hide the Full List of Drugs
Dactolisib
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [8]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug Dactolisib
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell proliferation Inhibition hsa05200
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
PNT2C2 cells Prostate Homo sapiens (Human) CVCL_4889
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
GAS5 assay; MTS assay
Mechanism Description First generation mTORC1, combined mTORC1/mTORC2 and dual PI3k/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 LncRNA sensitized PC-3 and DU 145 cells to these agents.
AZD-8055
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [8]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug AZD-8055
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell proliferation Inhibition hsa05200
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
PNT2C2 cells Prostate Homo sapiens (Human) CVCL_4889
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
GAS5 assay; MTS assay
Mechanism Description First generation mTORC1, combined mTORC1/mTORC2 and dual PI3k/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 LncRNA sensitized PC-3 and DU 145 cells to these agents.
Discontinued Drug(s)
1 drug(s) in total
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Urethane
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Regulation by the Disease Microenvironment (RTDM) Click to Show/Hide
Disease Class: Lung adenocarcinoma [14]
Resistant Disease Lung adenocarcinoma [ICD-11: 2C25.0]
Resistant Drug Urethane
Molecule Alteration Down-regulation
Interaction
Experimental Note Identified from the Human Clinical Data
In Vitro Model 16HBE cells Lung Homo sapiens (Human) CVCL_0112
In Vivo Model BALB/c nude mice model Mus musculus
Experiment for
Molecule Alteration
Overexpression assay
Experiment for
Drug Resistance
EdU assay
Mechanism Description Low Long Noncoding RNA Growth Arrest-Specific Transcript 5 Expression in the Exosomes of Lung Cancer Cells Promotes Tumor Angiogenesis.
Investigative Drug(s)
5 drug(s) in total
Click to Show/Hide the Full List of Drugs
Alpha-solanine
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [14]
Resistant Disease Prostate cancer [ICD-11: 2C82.0]
Resistant Drug Alpha-solanine
Molecule Alteration Down-regulation
Expression
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation GAS5/miR-18a signaling pathway Activation hsa05206
In Vitro Model RWPE-1 cells Prostate Homo sapiens (Human) CVCL_3791
DU145 cells Prostate Homo sapiens (Human) CVCL_0105
Experiment for
Molecule Alteration
Overexpression assay
Experiment for
Drug Resistance
CCK8 assay
Mechanism Description Long noncoding RNA GAS5 modulates alpha-Solanine-induced radiosensitivity by negatively regulating miR-18a in human prostate cancer cells.
Carbon tetrachloride
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Hepatic fibrosis [14]
Resistant Disease Hepatic fibrosis [ICD-11: DB93.0]
Resistant Drug Carbon tetrachloride
Molecule Alteration Down-regulation
Interaction
Experimental Note Discovered Using In-vivo Testing Model
In Vitro Model HSC cells N.A. . N.A.
In Vivo Model Rat hepatic fibrosis model Rattus norvegicus
Experiment for
Molecule Alteration
qRT-PCR; Western bloting analysis; Dual luciferase assay; RNA pull down assay
Mechanism Description LncRNA GAS5/miR-23a may bring molecular targets for hepatic fibrosis therapy.LncRNA GAS5 restrains CCl4-induced hepatic fibrosis by targeting miR-23a through the PTEN/PI3K/Akt signaling pathway.
Homocysteine
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Cardiac microvascular endothelial cells injury [14]
Resistant Disease Cardiac microvascular endothelial cells injury [ICD-11: BE2Z.Y]
Resistant Drug Homocysteine
Molecule Alteration Down-regulation
Interaction
Experimental Note Revealed Based on the Cell Line Data
In Vitro Model ECs N.A. Drosophila melanogaster (Fruit fly) CVCL_Z893
CMECs N.A. . N.A.
Experiment for
Molecule Alteration
Overexpression assay
Experiment for
Drug Resistance
MTT assay; EdU assay; TUNEL staining assay; Caspase-3 activity detection; Dual luciferase reporter gene assay
Mechanism Description Long-chain noncoding RNA GAS5 mediates oxidative stress in cardiac microvascular endothelial cells injury.
Nutlin-3
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Prostate cancer [6]
Resistant Disease Prostate cancer [ICD-11: 2C82.0]
Resistant Drug Nutlin-3
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Inhibition hsa04210
In Vitro Model PC3 cells Prostate Homo sapiens (Human) CVCL_0035
22RV1 cells Prostate Homo sapiens (Human) CVCL_1045
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Fluorescence microscopy test apoptosis assay
Mechanism Description Transient expression of GAS5 enhances apoptosis and decreases the survival of 22Rv1 cells, forced variation of GAS5 gene expression can modulate cellular responses to various apoptotic stimuli, including a range of chemotherapeutic drugs.
Orthocresol
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Melanoma [15]
Sensitive Disease Melanoma [ICD-11: 2C30.0]
Sensitive Drug Orthocresol
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
Cell proliferation Inhibition hsa05200
In Vitro Model A375 cells Skin Homo sapiens (Human) CVCL_0132
A431 cells Skin Homo sapiens (Human) CVCL_0037
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay; Flow cytometry assay
Mechanism Description 2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells. Overexpression of LncRNA GAS5 inhibited cell proliferation and promoted cell apoptosis in skin cancer cells.
Disease Class: Skin squamous cell carcinoma [15]
Sensitive Disease Skin squamous cell carcinoma [ICD-11: 2C31.2]
Sensitive Drug Orthocresol
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
Cell proliferation Inhibition hsa05200
In Vitro Model A375 cells Skin Homo sapiens (Human) CVCL_0132
A431 cells Skin Homo sapiens (Human) CVCL_0037
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
MTT assay; Flow cytometry assay
Mechanism Description 2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells. Overexpression of LncRNA GAS5 inhibited cell proliferation and promoted cell apoptosis in skin cancer cells.
Disease- and Tissue-specific Abundances of This Molecule
ICD Disease Classification 02
Click to Show/Hide the Resistance Disease of This Class
Pancreatic cancer [ICD-11: 2C10]
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Differential expression of molecule in resistant diseases
The Studied Tissue Pancreas
The Specified Disease Pancreatic adenocarcinoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 1.85E-20; Fold-change: 4.28E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Lung cancer [ICD-11: 2C25]
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Differential expression of molecule in resistant diseases
The Studied Tissue Lung
The Specified Disease Lung adenocarcinoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 1.08E-07; Fold-change: -1.65E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
The Studied Tissue Lung
The Specified Disease Lung squamous cell carcinoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 1.80E-04; Fold-change: -1.04E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Melanoma [ICD-11: 2C30]
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Differential expression of molecule in resistant diseases
The Studied Tissue Skin
The Specified Disease Skin cutaneous melanoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 3.82E-06; Fold-change: 1.17E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Cervical cancer [ICD-11: 2C77]
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Differential expression of molecule in resistant diseases
The Studied Tissue Cervix uteri
The Specified Disease Cervical and endocervical cancer
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 1.40E-04; Fold-change: 4.91E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Prostate cancer [ICD-11: 2C82]
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Differential expression of molecule in resistant diseases
The Studied Tissue Prostate
The Specified Disease Prostate adenocarcinoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 4.67E-11; Fold-change: -2.27E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Bladder cancer [ICD-11: 2C94]
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Differential expression of molecule in resistant diseases
The Studied Tissue Bladder
The Specified Disease Bladder urothelial carcinoma
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 2.10E-01; Fold-change: -1.18E-02
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Tissue-specific Molecule Abundances in Healthy Individuals
Click to Show/Hide the Molecule Abundances
References
Ref 1 Growth arrest-specific 5 attenuates cisplatin-induced apoptosis in cervical cancer by regulating STAT3 signaling via miR-21. J Cell Physiol. 2019 Jun;234(6):9605-9615. doi: 10.1002/jcp.27647. Epub 2018 Oct 23.
Ref 2 GAS5 knockdown reduces the chemo-sensitivity of non-small cell lung cancer (NSCLC) cell to cisplatin (DDP) through regulating miR-21/PTEN axis. Biomed Pharmacother. 2017 Sep;93:570-579. doi: 10.1016/j.biopha.2017.06.089. Epub 2017 Jul 4.
Ref 3 Long Noncoding RNA GAS5, Which Acts as a Tumor Suppressor via microRNA 21, Regulates Cisplatin Resistance Expression in Cervical Cancer. Int J Gynecol Cancer. 2017 Jul;27(6):1096-1108. doi: 10.1097/IGC.0000000000001028.
Ref 4 GAS5 modulated autophagy is a mechanism modulating cisplatin sensitivity in NSCLC cells. Eur Rev Med Pharmacol Sci. 2016 Jun;20(11):2271-7.
Ref 5 Long non-coding RNA GAS5 inhibits DDP-resistance and tumor progression of epithelial ovarian cancer via GAS5-E2F4-PARP1-MAPK axis. J Exp Clin Cancer Res. 2019 Aug 7;38(1):345. doi: 10.1186/s13046-019-1329-2.
Ref 6 Long non-coding RNA GAS5 regulates apoptosis in prostate cancer cell lines. Biochim Biophys Acta. 2013 Oct;1832(10):1613-23. doi: 10.1016/j.bbadis.2013.05.005. Epub 2013 May 12.
Ref 7 Long noncoding RNA GAS5 inhibits malignant proliferation and chemotherapy resistance to doxorubicin in bladder transitional cell carcinoma. Cancer Chemother Pharmacol. 2017 Jan;79(1):49-55. doi: 10.1007/s00280-016-3194-4. Epub 2016 Nov 22.
Ref 8 Reciprocal regulation of GAS5 lncRNA levels and mTOR inhibitor action in prostate cancer cells. Prostate. 2015 May;75(7):693-705. doi: 10.1002/pros.22952. Epub 2015 Feb 3.
Ref 9 Long non-coding RNA GAS5 antagonizes the chemoresistance of pancreatic cancer cells through down-regulation of miR-181c-5p. Biomed Pharmacother. 2018 Jan;97:809-817. doi: 10.1016/j.biopha.2017.10.157. Epub 2017 Nov 6.
Ref 10 The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. J Hematol Oncol. 2015 Apr 29;8:43. doi: 10.1186/s13045-015-0140-6.
Ref 11 lncRNA GAS5 Reverses EMT and Tumor Stem Cell-Mediated Gemcitabine Resistance and Metastasis by Targeting miR-221/SOCS3 in Pancreatic Cancer. Mol Ther Nucleic Acids. 2018 Dec 7;13:472-482. doi: 10.1016/j.omtn.2018.09.026. Epub 2018 Oct 6.
Ref 12 Role of GAS5 noncoding RNA in mediating the effects of rapamycin and its analogues on mantle cell lymphoma cells. Clin Lymphoma Myeloma Leuk. 2014 Dec;14(6):468-73. doi: 10.1016/j.clml.2014.02.011. Epub 2014 Mar 3.
Ref 13 Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer. Oncotarget. 2016 May 10;7(19):27778-86. doi: 10.18632/oncotarget.8413.
Ref 14 lncRNA GAS5 restrains CCl(4)-induced hepatic fibrosis by targeting miR-23a through the PTEN/PI3K/Akt signaling pathwayAm J Physiol Gastrointest Liver Physiol. 2019 Apr 1;316(4):G539-G550. doi: 10.1152/ajpgi.00249.2018. Epub 2019 Feb 8.
Ref 15 2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells. Cell Death Dis. 2017 Mar 2;8(3):e2638. doi: 10.1038/cddis.2017.66.

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