Background: As one of the leading cancer-related mortalities worldwide, colorectal cancer (CRC) shows resistance to chemotherapy mainly because of drug resistance. Existing evidence has revealed that long noncoding RNAs (lncRNAs) are related to tumorigenesis and chemoresistance scenarios. However, the mechanism by which lncRNA induces chemoresistance and the postoperative prognosis of CRC both remain unclear.
Methods: The expression of a lncRNA named lncARSR in CRC tissue was tested, and its association with clinical and pathological features was analyzed. Gain-of-function and loss-of-function assays were conducted to investigate the role of lncARSR in vivo and in vitro.
Results: Functional analysis showed that overexpressing lncARSR increased oxaliplatin (OXA) resistance of CRC cells in vitro and in vivo. Moreover, lncARSR conferred chemoresistance to CRC cells. Silencing lncARSR decreased cell viability and promoted cell apoptosis after OXA treatment, whereas overexpression of lncARSR increased cell viability and reduced cell apoptosis after OXA treatment. In addition, lncARSR overexpression induced the tumor formation capacity of colorectal cancer cells.
Conclusions: The results obtained in the present study show that up-regulation of lncARSR promoted OXA resistance in CRC. Our results also imply that lncARSR may be a candidate marker for CRC chemoresistance.
Keywords: chemotherapy; colon/rectal cancer; molecular genetics.
© 2020 John Wiley & Sons, Ltd.