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Identification of BRMS1L as Metastasis Suppressing Gene in Esophageal Squamous Cell Carcinoma

Authors Zhou R, Tang X, Li L, Zhang F, Sun J, Ju C, Zhou Y, Liu R, Liang Y, Lv B, Zhang Z, Hu H, Lv XB

Received 28 September 2019

Accepted for publication 4 January 2020

Published 23 January 2020 Volume 2020:12 Pages 531—539

DOI https://doi.org/10.2147/CMAR.S232632

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Chien-Feng Li


Ruihao Zhou, 1, 2,* Xiaofeng Tang, 1,* Liping Li, 3,* Feifei Zhang, 1 Jun Sun, 1 Cheng Ju, 1, 4 Yan Zhou, 5 Renfeng Liu, 1, 4 Yiping Liang, 1 Bin Lv, 1, 4 Zhiping Zhang, 1, 4 Haiyan Hu, 5 Xiao-Bin Lv 1

1Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The Third Affiliated Hospital of Nanchang University, Nanchang 30008, People’s Republic of China; 2Department of Pain Management, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China; 3Department of Clinical Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, People’s Republic of China; 4Department of Orthopedics, The Third Affiliated Hospital of Nanchang University,Nanchang 330008, People’s Republic of China; 5Department of Oncology,Shanghai Jiao Tong University Affiliated Sixth People’s Hospital of Shanghai, Shanghai 200233, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Xiao-Bin Lv
Jiangxi Key Laboratory of Cancer Metastasis and Precision Treatment, The Third Affiliated Hospital of Nanchang University, North 128 Xiangshan Road, Nanchang 30008, Jiangxi, People’s Republic of China
Email nclvxiaobin@sina.cn

Haiyan Hu
Department of Oncology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, No. 600 Yishan Road, Xuhui District, Shanghai City 200233, People’s Republic of China
Email xuri1104@163.com

Introduction: Breast cancer metastasis suppressor 1 like (BRMS1-like)was first reported to be a component of the Sin3-HDAC complex, but the role in the progression of cancers was largely unknown. Our previous study reported that BRMS1L promoted the metastasis of breast cancer through facilitating the recruitment of HDAC complex to the promoter FZD10, and hence suppressing the transcription of FZD10.
Methods: In this study, we detected the expression level of BRMS1L in esophageal squamous cell carcinoma (ESCC). The effect of BRMS1L in TE-1D (knockdown) and ECA-109 (overexpression) cell lines was explored by transwell assays, wound healing assays, and cell adhesion assays. Quantitative real‑time PCR, Western blot analysis, and luciferase assays were used to detect the interaction of the CBP/P300-BRMS1L-ITGA7 axis.
Results: In the present study, we found that knockdown of BRMS1L promoted the migration, invasion, and epithelial–mesenchymal transition (EMT). Conversely, overexpression of BRMS1L inhibited the migration and invasion of ESCC. Mechanistically, BRMS1L exerted their metastasis-suppressing role via transcriptionally repress ITGA7 expression. Moreover, we revealed that CBP/p 300 regulated the expression of BRMS1L and might be responsible for the down-regulation of BRMS1L in ESCC.
Conclusion: Collectively, we identified the role of CBP/p300-BRMS1L-ITGA7 axis in the metastasis of ESCC.

Keywords: BRMS1L, ESCC, EMT, ITGA7, CBP/P300, cell invasion and migration

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