General Information of the Molecule (ID: Mol01374)
Name
hsa-mir-30c ,Homo sapiens
Synonyms
microRNA 30c-2
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Molecule Type
Precursor miRNA
Gene Name
MIR30C2
Gene ID
407032
Location
chr6:71376960-71377031[-]
Sequence
AGAUACUGUAAACAUCCUACACUCUCAGCUGUGGAAAGUAAGAAAGCUGGGAGAAGGCUG
UUUACUCUUUCU
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Ensembl ID
ENSG00000199094
HGNC ID
HGNC:31627
Precursor Accession
MI0000254
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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)
2 drug(s) in total
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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: Breast cancer [1]
Resistant Disease Breast cancer [ICD-11: 2C60.3]
Resistant Drug Doxorubicin
Molecule Alteration Expression
Down-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation p38/MAPK signaling pathway Inhibition hsa04010
In Vitro Model MCF-7 cells Breast Homo sapiens (Human) CVCL_0031
MDA-MB-231 cells Breast Homo sapiens (Human) CVCL_0062
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
qRT-PCR
Experiment for
Drug Resistance
CCK8 assay
Mechanism Description Down-regulation of miR-30c correlated with overexpression of YWHAZ in breast doxorubicin-resistant cells, Overexpression of miR-30c sensitized MCF-7/ADR cells to doxorubicin, miR-30c suppressed expression of the YWHAZ gene, YWHAZ was a key signal molecule in doxorubicin resistance by reducing activation of the p38MAPk signal pathway in MCF-7/ADR cells, miR-30c regulated doxorubicin resistance in vivo.
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Regulation by the Disease Microenvironment (RTDM) Click to Show/Hide
Disease Class: Breast cancer [2]
Sensitive Disease Breast cancer [ICD-11: 2C60.3]
Sensitive Drug Doxorubicin
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
In Vitro Model MCF-7 cells Breast Homo sapiens (Human) CVCL_0031
MDA-MB-231 cells Breast Homo sapiens (Human) CVCL_0062
HEK293T cells Kidney Homo sapiens (Human) CVCL_0063
G418 cells Breast Homo sapiens (Human) N.A.
In Vivo Model NOD/SCID nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Flow cytometry assay
Mechanism Description miR-30c plays a pivotal role in Paclitaxel and Doxorubicin chemo-resistance by a direct targeting of TWF1, which encodes an actin-binding protein and promotes EMT.
Paclitaxel
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Regulation by the Disease Microenvironment (RTDM) Click to Show/Hide
Disease Class: Breast cancer [2]
Sensitive Disease Breast cancer [ICD-11: 2C60.3]
Sensitive Drug Paclitaxel
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell apoptosis Activation hsa04210
In Vitro Model MCF-7 cells Breast Homo sapiens (Human) CVCL_0031
MDA-MB-231 cells Breast Homo sapiens (Human) CVCL_0062
HEK293T cells Kidney Homo sapiens (Human) CVCL_0063
G418 cells Breast Homo sapiens (Human) N.A.
In Vivo Model NOD/SCID nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
Flow cytometry assay
Mechanism Description miR-30c plays a pivotal role in Paclitaxel and Doxorubicin chemo-resistance by a direct targeting of TWF1, which encodes an actin-binding protein and promotes EMT.
References
Ref 1 Involvement of miR-30c in resistance to doxorubicin by regulating YWHAZ in breast cancer cells. Braz J Med Biol Res. 2014 Jan;47(1):60-9. doi: 10.1590/1414-431X20133324. Epub 2014 Jan 10.
Ref 2 MicroRNA-30c inhibits human breast tumour chemotherapy resistance by regulating TWF1 and IL-11. Nat Commun. 2013;4:1393. doi: 10.1038/ncomms2393.

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