LncRNA CCAT1 enhances chemoresistance in hepatocellular carcinoma by targeting QKI-5

A major reason for treatment failure of cancer is acquisition of drug resistance. The specific mechanisms underlying hepatocellular carcinoma (HCC) chemoresistance need to be fully elucidated. lncRNAs involve in drug resistance in some cancers, however, the exact functions of lncRNA colon cancer-ass...

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Bibliographic Details
Published in:Scientific reports 2022-05, Vol.12 (1), p.7826-7826, Article 7826
Main Authors: Xia, Chongsheng, Sun, Yurui, Li, Yang, Ma, Junli, Shi, Jing
Format: Article
Language:English
Subjects:
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Apoptosis
Carcinoma, Hepatocellular - drug therapy
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Cell Line, Tumor
Cell Proliferation
Chemoresistance
Colon cancer
Colonic Neoplasms - genetics
Drug resistance
Drug Resistance, Neoplasm - genetics
Gene Expression Regulation, Neoplastic
Hepatocellular carcinoma
Humanities and Social Sciences
Humans
Liver cancer
Liver Neoplasms - drug therapy
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
MAP kinase
MicroRNAs - genetics
multidisciplinary
Non-coding RNA
Oxaliplatin
Oxaliplatin - pharmacology
Oxaliplatin - therapeutic use
p38 Mitogen-Activated Protein Kinases - metabolism
Qk protein
RNA, Long Noncoding - genetics
RNA-Binding Proteins - metabolism
Science
Science (multidisciplinary)
Signal transduction
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Summary:A major reason for treatment failure of cancer is acquisition of drug resistance. The specific mechanisms underlying hepatocellular carcinoma (HCC) chemoresistance need to be fully elucidated. lncRNAs involve in drug resistance in some cancers, however, the exact functions of lncRNA colon cancer-associated transcript 1 (CCAT1) in oxaliplatin resistance in HCC are still unknown. Our study indicated that CCAT1 promoted HCC proliferation and reduced the apoptosis induced by oxaliplatin. Knockout of CCAT1 could increased chemosensitivity in vitro and in vivo. Further study found that QKI-5 was an important mediator and blocking of QKI-5/p38 MAPK signaling pathway could enhance oxaliplatin sensitivity. In conclusions, CCAT1 promoted proliferation and oxaliplatin resistance via QKI-5/p38 MAPK signaling pathway in HCC. Targeting CCAT1 in combination with chemotherapeutics may be a promising alternative to reverse drug resistance in HCC treatment.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-022-11644-4