Abstract
The dysregulated expression of circRNA in gastric cancer (GC) induces paclitaxel (Tax) resistance of cancer cells, which in turn affects disease progression and prognosis. Here, we sought to investigate the role and mechanism of circ_002136 in Tax-resistant GC. In this study, we found the enriched circ_002136 level and the declined miR-16-5p level in Tax-resistant GC tissues and cells. Biologically, knockdown of circ_002136 elevated the Tax sensitivity of Tax-resistant GC cells, inhibited the cell motility properties, and simultaneously drove the apoptosis. Mechanically, circ_002136 promoted the HMGA1-mediated cellular Tax resistance and cell invasion by sponging miR-16-5p. Furthermore, circ_002136 silencing impeded the growth of Tax-resistant GC tumors in vivo. Overall, our study revealed a novel signaling pathway that could be used for future clinical applications, namely the circ_002136/miR-16-5p/HMGA1 axis to regulate the Tax resistance of GC cells.