BRMS1 Suppresses Lung Cancer Metastases through an E3 Ligase Function on Histone Acetyltransferase p300

Liu, Yuan; Mayo, Marty W.; Nagji, Alykhan S.; Hall, Emily H.; Shock, Lisa S.; Xiao, Aizhen; Stelow, Edward B.; Jones, David R.

doi:10.1158/0008-5472.can-12-2489

Cited by 37 publications

(35 citation statements)

References 43 publications

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“…In support of our observation regarding activation of selective EMT-TFs, Pantuck and colleagues demonstrated that loss of VHL activity stimulated renal cell carcinoma cells to activate NF-B and promote EMT through selective upregulation of Twist1 and Slug but not Snail, Zeb1, or Zeb2 (53). Interestingly, both BRMS1 and VHL can function as E3 ubiquitin ligases to suppress tumor progression (29,54). Therefore, one plausible explanation of these observations is that the targets of E3 ligases BRMS1 and VHL, such as p300 and HIF1␣, respectively, contribute to NF-B-mediated selective upregulation of Twist1.…”

Section: Discussionmentioning

confidence: 99%

“…BRMS1 has been shown to function as a corepressor to inhibit NF-B transactivation through deacetylation of the RelA/ p65 subunit at K310 (25). Additional mechanisms by which BRMS1 functions include the regulation of phosphoinositide signaling (26), expression of microRNA (miRNA) (27), angiogenesis (28), and p300 histone acetyltransferase levels (29). Whereas metastasis suppressor family members NM23, CD44, MKK4, and Kiss1 have been shown to regulate EMT, the role of BRMS1 in EMT has not been previously explored.…”

mentioning

confidence: 99%

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Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of Twist1

Liu

Mayo

Xiao

et al. 2015

Molecular and Cellular Biology

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of Twist1

Liu

Mayo

Xiao

et al. 2015

Molecular and Cellular Biology

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“…First identified in 2000 (16), the gene suppresses the metastasis of breast carcinoma cells to lungs and regional lymph nodes. Subsequent studies indicated that BRMS1 mediated inhibition of metastasis in multiple types of human cancer, including GC (17)(18)(19)(20). A number of studies have confirmed that a number of protein-coding genes are regulated by miR-125a-5p in different types of human cancer (21,22).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑125a‑5p inhibits invasion and metastasis of gastric cancer cells by targeting BRMS1 expression

Cao

Tan

et al. 2018

Oncol Lett

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Abstract. Accumulating studies have demonstrated microRNAs (miRNAs/miRs) have an important role in multiple processes of human malignant tumor development and progression. Decreased expression of miR-125a-5p has been observed in several types of cancer, including gastric cancer (GC). However, the mechanism and exact function of miR-125a-5p in GC have not been largely elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction indicated that the expression of miR-125a-5p was downregulated in GC tissues and cell lines compared with matched normal tissues (P<0.01) and normal gastric mucosa cell lines (P<0.01), respectively. Moreover, clinical pathological characteristics and Kaplan-Meier analysis indicated that a low expression of miR-125a-5p was not only associated with lymph metastasis, peritoneal dissemination and advanced tumor-node metastasis stage but also affected the prognosis of GC patients. Compared with miR-control-transfected GC cells, markedly decreased migration and invasion was observed in GC cells that overexpress miR-125a-5p. By contrast, increased metastasis and invasion were observed in miR-125a-5p-knocked down cells compared with the control. Furthermore, luciferase reporter assays indicated that breast cancer metastasis suppressor 1 (BRMS1) was a direct target of miR-125a-5p. Notably, a positive correlation between the levels of BRMS1 and miR-125a-5p in GC tissues was observed, and BRMS1 expression was indicated to be regulated by miR-125a-5p in GC cells. In conclusion, miR-125a-5p may act as a tumor suppressor by targeting the metastasis-inhibitory gene, BRMS1. The data suggesting that BRMS1 is a potential target gene of miR-125a-5p, may provide novel insight into miRNA regulation of human gene expression, and a useful target for gene therapy of GC.

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“…SIN3 proteins can link HDAC and co-repressors to chromatin-bound transcription factors to inhibit target gene expression 9,10 . Downregulation of breast cancer metastasis suppressor 1 (BRMS1), a major co-repressor interacting with Sin3A, is associated with metastasis of multiple types of malignancies, including breast, nasopharyngeal, melanoma, non-small-cell lung cancinomas and melanomas [11][12][13][14][15] . Moreover, transfection of BRMS1 into highly metastatic human breast cancer cell lines significantly inhibited lung metastasis in xenografted mice without influencing orthotopic tumour incidence and growth rate, suggesting that BRMS1 is a metastasis suppressor 16 .…”

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confidence: 99%

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Gong

et al. 2014

Nat Commun

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BRMS1L (breast cancer metastasis suppressor 1 like, BRMS1-like) is a component of Sin3A-histone deacetylase (HDAC) co-repressor complex that suppresses target gene transcription. Here we show that reduced BRMS1L in breast cancer tissues is associated with metastasis and poor patient survival. Functionally, BRMS1L inhibits breast cancer cells migration and invasion by inhibiting epithelial-mesenchymal transition. These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signalling, through HDAC1 recruitment and histone H3K9 deacetylation at the promoter. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10-b-catenin signalling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNA interference-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, whereas ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signalling in breast cancer cells and acts as a breast cancer metastasis suppressor.

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BRMS1 Suppresses Lung Cancer Metastases through an E3 Ligase Function on Histone Acetyltransferase p300

Cited by 37 publications

References 43 publications

Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of Twist1

Loss of BRMS1 Promotes a Mesenchymal Phenotype through NF-κB-Dependent Regulation of Twist1

MicroRNA‑125a‑5p inhibits invasion and metastasis of gastric cancer cells by targeting BRMS1 expression

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

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