miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4
Abstract 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 usi...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-04-01
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| Series: | Thoracic Cancer |
| Subjects: | |
| Online Access: | https://doi.org/10.1111/1759-7714.14336 |
| Summary: | Abstract 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. |
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| ISSN: | 1759-7706 1759-7714 |