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: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Wiley
2022-04-01
|
Series: | Thoracic Cancer |
Subjects: | |
Online Access: | https://doi.org/10.1111/1759-7714.14336 |
_version_ | 1811311696227074048 |
---|---|
author | Weizheng Zhou Chengliang Cai Jie Lu Qiao Fan |
author_facet | Weizheng Zhou Chengliang Cai Jie Lu Qiao Fan |
author_sort | Weizheng Zhou |
collection | DOAJ |
description | 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. |
first_indexed | 2024-04-13T10:23:28Z |
format | Article |
id | doaj.art-e9bce0a514994012bf010fabb9c5facd |
institution | Directory Open Access Journal |
issn | 1759-7706 1759-7714 |
language | English |
last_indexed | 2024-04-13T10:23:28Z |
publishDate | 2022-04-01 |
publisher | Wiley |
record_format | Article |
series | Thoracic Cancer |
spelling | doaj.art-e9bce0a514994012bf010fabb9c5facd2022-12-22T02:50:25ZengWileyThoracic Cancer1759-77061759-77142022-04-0113795696410.1111/1759-7714.14336miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4Weizheng Zhou0Chengliang Cai1Jie Lu2Qiao Fan3Department of Cardiothoracic Surgery Changhai Hospital, The Second Military Medical University Shanghai ChinaDepartment of Cardiothoracic Surgery Changhai Hospital, The Second Military Medical University Shanghai ChinaDepartment of Cardiothoracic Surgery Changhai Hospital, The Second Military Medical University Shanghai ChinaDepartment of Cardiothoracic Surgery Changhai Hospital, The Second Military Medical University Shanghai ChinaAbstract 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.https://doi.org/10.1111/1759-7714.14336cisplatinmiR‐129‐2NSCLCSOX4target |
spellingShingle | Weizheng Zhou Chengliang Cai Jie Lu Qiao Fan miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 Thoracic Cancer cisplatin miR‐129‐2 NSCLC SOX4 target |
title | miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 |
title_full | miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 |
title_fullStr | miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 |
title_full_unstemmed | miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 |
title_short | miR‐129‐2 upregulation induces apoptosis and promotes NSCLC chemosensitivity by targeting SOX4 |
title_sort | mir 129 2 upregulation induces apoptosis and promotes nsclc chemosensitivity by targeting sox4 |
topic | cisplatin miR‐129‐2 NSCLC SOX4 target |
url | https://doi.org/10.1111/1759-7714.14336 |
work_keys_str_mv | AT weizhengzhou mir1292upregulationinducesapoptosisandpromotesnsclcchemosensitivitybytargetingsox4 AT chengliangcai mir1292upregulationinducesapoptosisandpromotesnsclcchemosensitivitybytargetingsox4 AT jielu mir1292upregulationinducesapoptosisandpromotesnsclcchemosensitivitybytargetingsox4 AT qiaofan mir1292upregulationinducesapoptosisandpromotesnsclcchemosensitivitybytargetingsox4 |