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...

Full description

Bibliographic Details
Main Authors: Weizheng Zhou, Chengliang Cai, Jie Lu, Qiao Fan
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