Molecule Information
General Information of the Molecule (ID: Mol01330)
Name |
hsa-let-7c
,Homo sapiens
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Synonyms |
microRNA let-7c
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Molecule Type |
Precursor miRNA
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Gene Name |
MIRLET7C
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Gene ID | |||||
Location |
chr21:16539828-16539911[+]
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Sequence |
GCAUCCGGGUUGAGGUAGUAGGUUGUAUGGUUUAGAGUUACACCCUGGGAGUUAACUGUA
CAACCUUCUAGCUUUCCUUGGAGC Click to Show/Hide
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Ensembl ID | |||||
HGNC ID | |||||
Precursor Accession | |||||
Click to Show/Hide the Complete Species Lineage | |||||
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)
5 drug(s) in total
Cisplatin
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Oral cancer | [1] | |||
Sensitive Disease | Oral cancer [ICD-11: 2B6E.1] | |||
Sensitive Drug | Cisplatin | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | Cell viability | Inhibition | hsa05200 | |
In Vitro Model | GNM cells | Oral | Homo sapiens (Human) | CVCL_WL58 |
SAS cells | Oral | Homo sapiens (Human) | CVCL_1675 | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
MTT assay | |||
Mechanism Description | The inhibitory effect of let-7c on various stemness phenotypes was reverted by IL-8, indicating that lower expression of let-7c may confer higher cancer stemness through a failure to downregulate IL-8. | |||
Disease Class: Esophageal squamous cell carcinoma | [2] | |||
Sensitive Disease | Esophageal squamous cell carcinoma [ICD-11: 2B70.3] | |||
Sensitive Drug | Cisplatin | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Activation | hsa04210 | |
IL6/STAT3 signaling signaling pathway | Inhibition | hsa04659 | ||
In Vitro Model | TE8 cells | Esophageal | Homo sapiens (Human) | CVCL_1766 |
TE13 cells | Esophageal | Homo sapiens (Human) | CVCL_4463 | |
TE10 cells | Esophagus | Homo sapiens (Human) | CVCL_1760 | |
TE1 cells | Esophagus | Homo sapiens (Human) | CVCL_1759 | |
TE11 cells | Esophagus | Homo sapiens (Human) | CVCL_1761 | |
TE5 cells | Esophagus | Homo sapiens (Human) | CVCL_1764 | |
TE9 cells | Esophagus | Homo sapiens (Human) | CVCL_1767 | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
MTT assay | |||
Mechanism Description | Let-7c directly repressed cisplatin-activated interleukin (IL) -6/STAT3 prosurvival pathway, restored sensitivity to cisplatin and increased rate of apoptosis after exposure to cisplatin. |
Docetaxel
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Regulation by the Disease Microenvironment (RTDM) | ||||
Disease Class: Lung adenocarcinoma | [3] | |||
Resistant Disease | Lung adenocarcinoma [ICD-11: 2C25.0] | |||
Resistant Drug | Docetaxel | |||
Molecule Alteration | Expression | Down-regulation |
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Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Cell invasion | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
Cell proliferation | Activation | hsa05200 | ||
In Vitro Model | SPC-A1 cells | Lung | Homo sapiens (Human) | CVCL_6955 |
H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 | |
In Vivo Model | Nude mouse xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
MTT assay; Colony formation assay; Tunel assay | |||
Mechanism Description | Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells.the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells. |
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Regulation by the Disease Microenvironment (RTDM) | ||||
Disease Class: Lung adenocarcinoma | [3] | |||
Sensitive Disease | Lung adenocarcinoma [ICD-11: 2C25.0] | |||
Sensitive Drug | Docetaxel | |||
Molecule Alteration | Expression | Up-regulation |
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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 | ||
In Vitro Model | SPC-A1 cells | Lung | Homo sapiens (Human) | CVCL_6955 |
H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 | |
In Vivo Model | Nude mouse xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
MTT assay; Colony formation assay; Tunel assay | |||
Mechanism Description | Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells.the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells. | |||
Disease Class: Lung adenocarcinoma | [4] | |||
Sensitive Disease | Lung adenocarcinoma [ICD-11: 2C25.0] | |||
Sensitive Drug | Docetaxel | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Caspase-3 signaling pathway | Activation | hsa04210 | |
Cell migration | Inhibition | hsa04670 | ||
In Vitro Model | SPC-A1 cells | Lung | Homo sapiens (Human) | CVCL_6955 |
H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 | |
In Vivo Model | BALB/c nude mouse xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
MTT assay | |||
Mechanism Description | Ectopic Let-7c expression could increase the sensitivity of docetaxel-resistant LAD cells to chemotherapeutic agents or irradiation and reverse their EMT phenotype by targeting Bcl-xL. |
Erlotinib
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Lung adenocarcinoma | [5] | |||
Sensitive Disease | Lung adenocarcinoma [ICD-11: 2C25.0] | |||
Sensitive Drug | Erlotinib | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Hedgehog signaling pathway | Inhibition | hsa04340 | |
In Vitro Model | A549 cells | Lung | Homo sapiens (Human) | CVCL_0023 |
H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 | |
Experiment for Molecule Alteration |
RT-PCR | |||
Experiment for Drug Resistance |
MTT assay | |||
Mechanism Description | miR-200b and let-7c, inhibited the TGF-beta1-mediated resistance of NSCLC cells to erlotinib. |
Gefitinib
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Non-small cell lung cancer | [6] | |||
Sensitive Disease | Non-small cell lung cancer [ICD-11: 2C25.Y] | |||
Sensitive Drug | Gefitinib | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | ERK signaling pathway | Inhibition | hsa04210 | |
PI3K/AKT signaling pathway | Inhibition | hsa04151 | ||
In Vitro Model | H1975 cells | Lung | Homo sapiens (Human) | CVCL_1511 |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
CCK8 assay | |||
Mechanism Description | The upregulation of let-7c was associated with the increased gefitinib sensitivity of H1975 cells, and that this effect was mediated by repression of the RAS oncogene and inactivation of the phosphoinositide 3-kinase (PI3k) /AkT and mitogen-activated extracellular signal-regulated kinase (MEk) /extracellular signal-regulated kinase (ERk) signaling pathways. |
Gemcitabine
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Regulation by the Disease Microenvironment (RTDM) | ||||
Disease Class: Pancreatic cancer | [7] | |||
Sensitive Disease | Pancreatic cancer [ICD-11: 2C10.3] | |||
Sensitive Drug | Gemcitabine | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | MIA PaCa-2 cells | Pancreas | Homo sapiens (Human) | CVCL_0428 |
PANC-1 cells | Pancreas | Homo sapiens (Human) | CVCL_0480 | |
AsPC-1 cells | Pancreas | Homo sapiens (Human) | CVCL_0152 | |
Experiment for Molecule Alteration |
RT-PCR | |||
Experiment for Drug Resistance |
WST-1 assay | |||
Mechanism Description | The expression of miR-200b, miR-200c, let-7b, let-7c, let-7d, and let-7e was significantly down-regulated in gemcitabine-resistant cells that showed EMT characteristics such as elongated fibroblastoid morphology, lower expression of epithelial marker E-cadherin, and higher expression of mesenchymal markers such as vimentin and ZEB1. |
References
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