ArticleCancer management and research2020
Identification of BRMS1L as Metastasis Suppressing Gene in Esophageal Squamous Cell Carcinoma.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanistic insights into miR-4775-mediated regulation of pancreatic cancer cell invasion and migration through BRMS1L.Hereditas · 2026Article
- BRMS1L promotes chemotherapy sensitivity by inhibiting autophagy in breast cancer.Frontiers in genetics · 2025Article
- Machine learning-identified stemness features and constructed stemness-related subtype with prognosis, chemotherapy, and immunotherapy responses for non-small cell lung cancer patients.Stem cell research & therapy · 2023Article
- Cancer chemoprevention through Frizzled receptors and EMT.Discover oncology · 2021Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBreast 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.
methodsIn 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.
resultsIn 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.
conclusionCollectively, we identified the role of CBP/p300-BRMS1L-ITGA7 axis in the metastasis of ESCC.
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