ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5
Abstract Cigarette smoking is an important risk factor in lung cancer development. As a class of regulatory RNAs, microRNAs (miRs) participate in various biological processes. In the present study, we searched for the key miRs that mediate cigarette smoke-induced aggressive phenotype in human bronch...
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BMC
2025-05-01
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| Series: | BMC Pulmonary Medicine |
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| Online Access: | https://doi.org/10.1186/s12890-025-03718-6 |
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| author | Kang-liang Zhang Dan-ni Wu Rui-heng Chen Chong Zheng Ri-sheng Huang Xiao-dan Zhao |
| author_facet | Kang-liang Zhang Dan-ni Wu Rui-heng Chen Chong Zheng Ri-sheng Huang Xiao-dan Zhao |
| author_sort | Kang-liang Zhang |
| collection | DOAJ |
| description | Abstract Cigarette smoking is an important risk factor in lung cancer development. As a class of regulatory RNAs, microRNAs (miRs) participate in various biological processes. In the present study, we searched for the key miRs that mediate cigarette smoke-induced aggressive phenotype in human bronchial epithelial (HBE) cells. Our results demonstrated that miR-652 was upregulated in cigarette smoke extract (CSE)-exposed HBE cells. ARID1A silencing due to hypermethylation of its promoter accounted for the upregulation of miR-652 in CSE-treated HBE cells. Overexpression of miR-652 accelerated the proliferation, migration, and anchorage-independent growth of HBE cells exposed to CSE. Knockdown of miR-652 attenuated the growth and migration of CSE-treated HBE cells. According to bioinformatic prediction and luciferase reporter assays, ZFAND5 was found to be a target of miR-652. Overexpression of miR-652 suppressed the protein expression of ZFAND5 in HBE cells, without altering its mRNA abundance. CSE treatment reduced the protein expression of ZFAND5 in HBE cells. Depletion of ZFAND5 potentiated the anchorage-independent growth and migration of CSE-treated HBE cells. Enforced expression of ZFAND5 reversed miR-652-mediated enhancement of anchorage-independent growth and migration in CSE-treated HBE cells. In conclusion, miR-652 potentiates CSE-induced aggressive phenotype in HBE cells by repressing ZFAND5 protein expression. The potential involvement of miR-652 in cigarette smoking-related lung carcinogenesis warrants further investigation. |
| format | Article |
| id | doaj-art-8454e06efae441c0b07d760219285a41 |
| institution | DOAJ |
| issn | 1471-2466 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | BMC |
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| series | BMC Pulmonary Medicine |
| spelling | doaj-art-8454e06efae441c0b07d760219285a412025-08-20T03:08:22ZengBMCBMC Pulmonary Medicine1471-24662025-05-0125111310.1186/s12890-025-03718-6ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5Kang-liang Zhang0Dan-ni Wu1Rui-heng Chen2Chong Zheng3Ri-sheng Huang4Xiao-dan Zhao5Department of Central Lab, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalDepartment of Thoracic Surgery, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalDepartment of Thoracic Surgery, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalDepartment of Thoracic Surgery, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalDepartment of Thoracic Surgery, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalDepartment of Nursing, The Dingli Clinical College of Wenzhou Medical University, Wenzhou Central HospitalAbstract Cigarette smoking is an important risk factor in lung cancer development. As a class of regulatory RNAs, microRNAs (miRs) participate in various biological processes. In the present study, we searched for the key miRs that mediate cigarette smoke-induced aggressive phenotype in human bronchial epithelial (HBE) cells. Our results demonstrated that miR-652 was upregulated in cigarette smoke extract (CSE)-exposed HBE cells. ARID1A silencing due to hypermethylation of its promoter accounted for the upregulation of miR-652 in CSE-treated HBE cells. Overexpression of miR-652 accelerated the proliferation, migration, and anchorage-independent growth of HBE cells exposed to CSE. Knockdown of miR-652 attenuated the growth and migration of CSE-treated HBE cells. According to bioinformatic prediction and luciferase reporter assays, ZFAND5 was found to be a target of miR-652. Overexpression of miR-652 suppressed the protein expression of ZFAND5 in HBE cells, without altering its mRNA abundance. CSE treatment reduced the protein expression of ZFAND5 in HBE cells. Depletion of ZFAND5 potentiated the anchorage-independent growth and migration of CSE-treated HBE cells. Enforced expression of ZFAND5 reversed miR-652-mediated enhancement of anchorage-independent growth and migration in CSE-treated HBE cells. In conclusion, miR-652 potentiates CSE-induced aggressive phenotype in HBE cells by repressing ZFAND5 protein expression. The potential involvement of miR-652 in cigarette smoking-related lung carcinogenesis warrants further investigation.https://doi.org/10.1186/s12890-025-03718-6Cigarette smokingLung epithelial cellmiR-652TransformationZFAND5 |
| spellingShingle | Kang-liang Zhang Dan-ni Wu Rui-heng Chen Chong Zheng Ri-sheng Huang Xiao-dan Zhao ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 BMC Pulmonary Medicine Cigarette smoking Lung epithelial cell miR-652 Transformation ZFAND5 |
| title | ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 |
| title_full | ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 |
| title_fullStr | ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 |
| title_full_unstemmed | ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 |
| title_short | ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5 |
| title_sort | arid1a silencing mediated upregulation of microrna 652 accelerates cigarette smoke induced human bronchial epithelial cell transformation by targeting zfand5 |
| topic | Cigarette smoking Lung epithelial cell miR-652 Transformation ZFAND5 |
| url | https://doi.org/10.1186/s12890-025-03718-6 |
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