LINC00525 targeting miR-338-3p promotes apoptosis and reduces paclitaxel resistance in gastric cancer cells

Abstract

Objective To study the effect of modulating the expression of LINC00525 targeting miR-338-3p on apoptosis and drug resistance of gastric cancer cells. Methods Paclitaxel-resistant gastric cancer cells (HGC-27/PTX) were transfected with si-NC, si-LINC00525, miR-NC, miR-338-3p, si-LINC00525+anti-miR-NC, or si-LINC00525+anti-miR-338-3p. Cell counting kit 8 (CCK-8) was used to determine the cell survival rate after the treatments. Real-time fluorescence quantitative PCR (RT-qPCR) was performed to detect LINC00525 and miR-338-3p expression levels, and Western blotting was used to detect the protein expression in the cells. The changes in cell apoptosis and migration and invasion abilities were analyzed using annexin V-FITC/PI double staining and Transwell assays. Dual luciferase reporter assay was performed to verify the targeting relationship between LINC00525 and miR-338-3p. Results The expression of LINC00525 was increased and that of miR-338-3p was decreased in both in HGC-27 and HGC-27/PTX cells. Knocking down LINC00525 and overexpression of miR-338-3p significantly increased the expression of caspase-3, P21, and E-cadherin, lowered the expression of MMP-2, decreased the cell survival rate, increased the cell apoptotic rate, and suppressed cell migration and invasion. Dual luciferase reporter assay showed that LINC00525 was capable of regulating the targeted miR-338-3p, and inhibition of miR-338-3p obviously attenuated the effects of LINC00525 knockdown on the survival, migration, invasion, and apoptosis of HGC-27/PTX cells. Conclusion LINC00525 knockdown can inhibit the proliferation, migration and invasion, promote apoptosis and reduce paclitaxel resistance of HGC-27/PTX cells by up-regulating miR-338-3.

Keywords

• linc00525
• mir-338-3p
• gastric cancer cells
• proliferation
• migration
• invasion
• apoptosis
• drug resistance