CircANKRD28 inhibits cisplatin resistance in non-small-cell lung cancer through the miR-221-3p/SOCS3 axis.

Abstract

Non-small-cell lung cancer (NSCLC) is a common cancer. Chemotherapeutic drug resistance limits the therapeutic effect of NSCLC and leads to a poor prognosis. As a result, new specific targets may be better identified by studying the mechanism of drug resistance to cisplatin in NSCLC. In the present study, we performed a quantitative real-time polymerase chain reaction and western blotting to detect mRNA and protein levels. The proliferation of cells was analyzed by a Cell Counting Kit-8 and colony formation assays. Cell invasion was measured via the Transwell assay. A scratch assay was performed to measure cell migration in cisplatin (DDP)-resistant NSCLC cells. Apoptosis of cells was examined using flow cytometry. We found that circANKRD28 was notably decreased in NSCLC. The results showed that circANKRD28 expression was not affected, and its half-life was more than 12 h. Functional experiments revealed that circANKRD28 overexpression inhibited DDP resistance in NSCLC cells in vitro. Mechanistic findings demonstrated that circANKRD28 regulated tumor cell progression and DDP sensitivity through the miR-221-3p/SOCS3 axis. The present study revealed the regulatory effects and molecular mechanism of circANKRD28 on the development and cisplatin resistance in NSCLC, which may provide experimental basis and theoretical support to identify new targets for therapy of DDP resistance in NSCLC.