miR-129-2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4.

Background: As one of the main causes of death worldwide, the treatment of non-small-cell lung cancer (NSCLC) is still unsatisfactory. This study aimed to explore the role of miR-129-2 in cell apoptosis and NSCLC chemosensitivity.

Methods: The effect of miR-129-2 on NSCLC was investigated using lung cancer cell lines (A549, NCl-H23, and HCC827), a normal lung cell line (BEAS-2B), and NSCLC tissues and adjacent healthy tissues. The oncogene SOX4 was verified as the target gene of miR-129-2 by luciferase reporter assay and real-time polymerase chain reaction.

Results: miR-129-2 expression was downregulated in NSCLC tissues, NCl-H23 cells, and A549 cells. miR-129-2 upregulation induced apoptosis in NCl-H23 and A549 cells. miR-129-2 upregulation also inhibited NSCLC in a xenograft mouse model, which was related to downregulation of SOX4 expression. Furthermore, miR-129-2 and SOX4 were aberrantly expressed in the cisplatin-resistant lung cancer cell line A549/DDP, and upregulation of miR-129-2 expression promoted cisplatin sensitivity in A549/DDP cells.

Conclusions: In conclusion, miR-129-2 expression was downregulated in NSCLC tissues and cell lines, and its upregulation induced cell apoptosis and promoted NSCLC chemosensitivity by regulating SOX4. Therefore, miR-129-2 can serve as a potential diagnostic and therapeutic target in NSCLC.