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CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling

BACKGROUND: Breast cancer is the major cause of death in females globally. Chemokine-like factor like MARVEL transmembrane domain containing 7 (CMTM7) is reported as a tumor suppressor and is involved in epidermal growth factor receptor degradation and PI3K/AKT signaling in previous studies. However...

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Autores principales: Chen, Zhao-Hui, Tian, Yao, Zhou, Guang-Lei, Yue, Hao-Ran, Zhou, Xue-Jie, Ma, Hai-Yan, Ge, Jie, Wang, Xin, Cao, Xu-Chen, Yu, Yue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960403/
https://www.ncbi.nlm.nih.gov/pubmed/36829181
http://dx.doi.org/10.1186/s13058-023-01620-9
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author Chen, Zhao-Hui
Tian, Yao
Zhou, Guang-Lei
Yue, Hao-Ran
Zhou, Xue-Jie
Ma, Hai-Yan
Ge, Jie
Wang, Xin
Cao, Xu-Chen
Yu, Yue
author_facet Chen, Zhao-Hui
Tian, Yao
Zhou, Guang-Lei
Yue, Hao-Ran
Zhou, Xue-Jie
Ma, Hai-Yan
Ge, Jie
Wang, Xin
Cao, Xu-Chen
Yu, Yue
author_sort Chen, Zhao-Hui
collection PubMed
description BACKGROUND: Breast cancer is the major cause of death in females globally. Chemokine-like factor like MARVEL transmembrane domain containing 7 (CMTM7) is reported as a tumor suppressor and is involved in epidermal growth factor receptor degradation and PI3K/AKT signaling in previous studies. However, other molecular mechanisms of CMTM7 remain unclear. METHODS: The expression level of CMTM7 in breast cancer cells and tissues was detected by qRT-PCR and western blot, and the methylation of CMTM7 promoter was detected by BSP sequencing. The effect of CMTM7 was verified both in vitro and in vivo, including MTT, colony formation, EdU assay, transwell assay and wound healing assay. The interaction between CMTM7 and CTNNA1 was investigated by co-IP assay. The regulation of miR-182-5p on CMTM7 and TCF3 on miR-182-5p was detected by luciferase reporter assay and ChIP analysis. RESULTS: This study detected the hypermethylation levels of the CMTM7 promoter region in breast cancer tissues and cell lines. CMTM7 was performed as a tumor suppressor both in vitro and in vivo. Furthermore, CMTM7 was a direct miR-182-5p target. Besides, we found that CMTM7 could interact with Catenin Alpha 1 (CTNNA1) and regulate Wnt/β-catenin signaling. Finally, transcription factor 3 (TCF3) can regulate miR-182-5p. We identified a feedback loop with the composition of miR-182-5p, CMTM7, CTNNA1, CTNNB1 (β-catenin), and TCF3, which play essential roles in breast cancer progression. CONCLUSION: These findings reveal the emerging character of CMTM7 in Wnt/β-catenin signaling and bring new sights of gene interaction. CMTM7 and other elements in the feedback loop may serve as emerging targets for breast cancer therapy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13058-023-01620-9.
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spelling pubmed-99604032023-02-26 CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling Chen, Zhao-Hui Tian, Yao Zhou, Guang-Lei Yue, Hao-Ran Zhou, Xue-Jie Ma, Hai-Yan Ge, Jie Wang, Xin Cao, Xu-Chen Yu, Yue Breast Cancer Res Research BACKGROUND: Breast cancer is the major cause of death in females globally. Chemokine-like factor like MARVEL transmembrane domain containing 7 (CMTM7) is reported as a tumor suppressor and is involved in epidermal growth factor receptor degradation and PI3K/AKT signaling in previous studies. However, other molecular mechanisms of CMTM7 remain unclear. METHODS: The expression level of CMTM7 in breast cancer cells and tissues was detected by qRT-PCR and western blot, and the methylation of CMTM7 promoter was detected by BSP sequencing. The effect of CMTM7 was verified both in vitro and in vivo, including MTT, colony formation, EdU assay, transwell assay and wound healing assay. The interaction between CMTM7 and CTNNA1 was investigated by co-IP assay. The regulation of miR-182-5p on CMTM7 and TCF3 on miR-182-5p was detected by luciferase reporter assay and ChIP analysis. RESULTS: This study detected the hypermethylation levels of the CMTM7 promoter region in breast cancer tissues and cell lines. CMTM7 was performed as a tumor suppressor both in vitro and in vivo. Furthermore, CMTM7 was a direct miR-182-5p target. Besides, we found that CMTM7 could interact with Catenin Alpha 1 (CTNNA1) and regulate Wnt/β-catenin signaling. Finally, transcription factor 3 (TCF3) can regulate miR-182-5p. We identified a feedback loop with the composition of miR-182-5p, CMTM7, CTNNA1, CTNNB1 (β-catenin), and TCF3, which play essential roles in breast cancer progression. CONCLUSION: These findings reveal the emerging character of CMTM7 in Wnt/β-catenin signaling and bring new sights of gene interaction. CMTM7 and other elements in the feedback loop may serve as emerging targets for breast cancer therapy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13058-023-01620-9. BioMed Central 2023-02-24 2023 /pmc/articles/PMC9960403/ /pubmed/36829181 http://dx.doi.org/10.1186/s13058-023-01620-9 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Chen, Zhao-Hui
Tian, Yao
Zhou, Guang-Lei
Yue, Hao-Ran
Zhou, Xue-Jie
Ma, Hai-Yan
Ge, Jie
Wang, Xin
Cao, Xu-Chen
Yu, Yue
CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title_full CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title_fullStr CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title_full_unstemmed CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title_short CMTM7 inhibits breast cancer progression by regulating Wnt/β-catenin signaling
title_sort cmtm7 inhibits breast cancer progression by regulating wnt/β-catenin signaling
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960403/
https://www.ncbi.nlm.nih.gov/pubmed/36829181
http://dx.doi.org/10.1186/s13058-023-01620-9
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