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-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.

Automated summary

Acquisition of drug resistance is a major reason for treatment failure in cancer. Long non-coding RNA (CCAT1) plays an important role in oxaliplatin resistance in hepatocellular carcinoma. The study found that CCAT1 promotes HCC proliferation and resistance to oxaliplatin through the QKI-5/p38 MAPK signaling pathway. Targeting CCAT1 may be a promising strategy to reverse drug resistance in HCC treatment.