TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer

Abstract Background FAM83A plays a significant role in the development of non-small cell lung cancer (NSCLC). This study elucidated the biological role of FAM83A in ferroptosis and cisplatin (DDP) sensitivity in NSCLC cells. Methods The expression patterns of FAM83A and TFAP2A were analyzed by bioin...

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Main Authors: Qi Sun, Weifeng Qu, Ye Wang, Kejia Yang, Yuan Weng
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Cell Division
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Online Access:https://doi.org/10.1186/s13008-025-00162-0
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author Qi Sun
Weifeng Qu
Ye Wang
Kejia Yang
Yuan Weng
author_facet Qi Sun
Weifeng Qu
Ye Wang
Kejia Yang
Yuan Weng
author_sort Qi Sun
collection DOAJ
description Abstract Background FAM83A plays a significant role in the development of non-small cell lung cancer (NSCLC). This study elucidated the biological role of FAM83A in ferroptosis and cisplatin (DDP) sensitivity in NSCLC cells. Methods The expression patterns of FAM83A and TFAP2A were analyzed by bioinformatic analysis. mRNA and protein levels were detected by quantitative PCR, immunoblotting, and immunohistochemistry, respectively. Cell invasion, migration, and viability were assessed by transwell, wound healing, CCK-8 assays, respectively. Cell ferroptosis was evaluated by measuring the levels of ROS, Fe2+, MDA, GSH, and SOD. Chromatin immunoprecipitation (ChIP) and luciferase assays were used to confirm the relationship between TFAP2A and the FAM83A promoter. Xenograft models were generated to evaluate the role of TFAP2A in vivo. Results FAM83A and TFAP2A levels were upregulated in human NSCLC. FAM83A inhibition decreased NSCLC cell growth, motility, and invasiveness, while inducing ferroptosis and enhancing DDP sensitivity. Mechanistically, TFAP2A regulated FAM83A transcription in NSCLC cells. TFAP2A depletion suppressed the malignant behaviors of NSCLC cells and augmented their sensitivity to ferroptosis and DDP, and these effects were reversed by the upregulation of FAM83A. Additionally, TFAP2A depletion decreased the growth of A549 subcutaneous xenografts in vivo. Moreover, the TFAP2A/FAM83A cascade regulated the activation of the PI3K/AKT and Wnt/β-catenin pathways. Conclusion Our study demonstrates that the novel TFAP2A/FAM83A cascade modulates ferroptosis and drug sensitivity in NSCLC.
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spelling doaj-art-0ee72adf6b9d4644be7132c31871c94e2025-08-20T04:03:07ZengBMCCell Division1747-10282025-07-0120111510.1186/s13008-025-00162-0TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancerQi Sun0Weifeng Qu1Ye Wang2Kejia Yang3Yuan Weng4Department of Thoracic Surgery, Affiliated Hospital of Jiangnan UniversityDepartment of Thoracic Surgery, Affiliated Hospital of Jiangnan UniversityDepartment of General Surgery, Haici Hospital Affiliated to Qingdao UniversityDepartment of Thoracic Surgery, Affiliated Hospital of Jiangnan UniversityDepartment of Thoracic Surgery, Affiliated Hospital of Jiangnan UniversityAbstract Background FAM83A plays a significant role in the development of non-small cell lung cancer (NSCLC). This study elucidated the biological role of FAM83A in ferroptosis and cisplatin (DDP) sensitivity in NSCLC cells. Methods The expression patterns of FAM83A and TFAP2A were analyzed by bioinformatic analysis. mRNA and protein levels were detected by quantitative PCR, immunoblotting, and immunohistochemistry, respectively. Cell invasion, migration, and viability were assessed by transwell, wound healing, CCK-8 assays, respectively. Cell ferroptosis was evaluated by measuring the levels of ROS, Fe2+, MDA, GSH, and SOD. Chromatin immunoprecipitation (ChIP) and luciferase assays were used to confirm the relationship between TFAP2A and the FAM83A promoter. Xenograft models were generated to evaluate the role of TFAP2A in vivo. Results FAM83A and TFAP2A levels were upregulated in human NSCLC. FAM83A inhibition decreased NSCLC cell growth, motility, and invasiveness, while inducing ferroptosis and enhancing DDP sensitivity. Mechanistically, TFAP2A regulated FAM83A transcription in NSCLC cells. TFAP2A depletion suppressed the malignant behaviors of NSCLC cells and augmented their sensitivity to ferroptosis and DDP, and these effects were reversed by the upregulation of FAM83A. Additionally, TFAP2A depletion decreased the growth of A549 subcutaneous xenografts in vivo. Moreover, the TFAP2A/FAM83A cascade regulated the activation of the PI3K/AKT and Wnt/β-catenin pathways. Conclusion Our study demonstrates that the novel TFAP2A/FAM83A cascade modulates ferroptosis and drug sensitivity in NSCLC.https://doi.org/10.1186/s13008-025-00162-0NSCLCFerroptosisDrug resistanceFAM83ATranscription factor
spellingShingle Qi Sun
Weifeng Qu
Ye Wang
Kejia Yang
Yuan Weng
TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
Cell Division
NSCLC
Ferroptosis
Drug resistance
FAM83A
Transcription factor
title TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
title_full TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
title_fullStr TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
title_full_unstemmed TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
title_short TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer
title_sort tfap2a upregulates fam83a to suppress ferroptosis and diminish cisplatin sensitivity in non small cell lung cancer
topic NSCLC
Ferroptosis
Drug resistance
FAM83A
Transcription factor
url https://doi.org/10.1186/s13008-025-00162-0
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