Mechanism of LncHOTAIR Regulating Proliferation, Apoptosis, and Autophagy of Lymphoma Cells through hsa-miR-6511b-5p/ATG7 Axis.

Objective: To explore the role of LncHOTAIR in apoptosis and autophagy in lymphoma. Methods: The interaction between LncHOTAIR and miR-6511b-5p, as well as between miR-6511b-5p and ATG7, was verified by a dual luciferase assay. LncHOTAIR overexpression lentivirus was transducted and siATG7s were transfected into Raji and BJAB lymphoma cells, and the efficiency was verified by qPCR. Lymphocyte proliferation was detected by the cell counting kit-8 (CCK8) test, and autophagy was detected by transmission electron microscopy. The protein expressions of ULK1, Beclin1, ATG7, LC3, Bax, cleaved-caspase 3, and Bcl-2 were detected using Western blots. Results: There was a targeting relationship between LncHOTAIR and miR-6511b-5p and between miR-6511b-5p and ATG7. LncHOTAIR overexpression promoted the proliferation and autophagy of Raji and BJAB cells, significantly upregulated ATG7, Beclin1, ULK1, Bcl-2, and LC3-II/LC3-I levels, and downregulated Bax and cleaved-caspase3 levels. siATG7 significantly inhibited the proliferation and autophagy of Raji and BJAB cells and promoted their apoptosis. Conclusion: LncHOTAIR/hsa-miR-6511b-5p/ATG7 could regulate the proliferation, apoptosis, and autophagy of Raji and BJAB lymphoma cells.

miR­29a suppresses IL­13­induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells.

IL­13 is a proinflammatory cytokine associated with multiple pathological conditions and the promotion of metastasis in lung cancer. Previous studies have demonstrated that IL­13 and YY1 are associated with PI3K/AKT signaling. In addition, miR­29a has been found to play a critical role in cell invasion in lung cancer. However, the molecular mechanism of miR­29a underlying its involvement in IL­13­induced lung cancer cell invasion remains largely unknown. In the present study, we aimed to investigate the role of miR­29a in cell invasion mediated by IL­13 in lung cancer. By using MTT and wound­scratch assays, we assessed cell proliferation and migration induced by IL­13, and identified activation of the PI3K/AKT/YY1 pathway. Inhibition of PI3K/AKT by LY294002 downregulated IL­13­induced YY1 expression. Furthermore, we found that miR­29a directly targets YY1 and suppressed its expression in lung cancer. By using MTT, flow cytometry and Transwell assays, overexpression of miR­29a restricted both YY1 and N­cadherin expression, and inhibited IL­13­induced invasion of lung cancer A549 cells. Taken together, these findings demonstrate that PI3K/AKT/YY1 is involved in the regulation of lung cancer cell behavior induced by IL­13, and miR­29a represents a promising therapeutic target.