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Last update 08 May 2025

BRMS1

Last update 08 May 2025

Basic Info

Synonyms

Breast cancer metastasis-suppressor 1, BRMS1, BRMS1 transcriptional repressor and anoikis regulator

+ [1]

Introduction

Transcriptional repressor. Down-regulates transcription activation by NF-kappa-B by promoting the deacetylation of RELA at 'Lys-310'. Promotes HDAC1 binding to promoter regions. Down-regulates expression of anti-apoptotic genes that are controlled by NF-kappa-B. Promotes apoptosis in cells that have inadequate adherence to a substrate, a process called anoikis, and may thereby inhibit metastasis. May be a mediator of metastasis suppression in breast carcinoma.

Drugs associated with BRMS1

Withaferin A

Target

ADAM8 x ANGPTL2 x BRMS1 x CSF-1R x HSP90 x IL-6 x TWEAK x tPA x uPA

Mechanism

ADAM8 antagonists [+8]

Active Org.

University of Louisville

Originator Org.

University of Louisville

Active Indication

Recurrent ovarian cancer

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with BRMS1

NCT05610735

/ RecruitingPhase 1/2IIT

Combination Therapy with Liposomal Doxorubicin and Withaferin a (Ashwagandha, ASWD) in Recurrent Ovarian Cancer

The proposed study "combination therapy with liposomal doxorubicin and withaferin A (Ashwagandha, ASWD) in recurrent ovarian cancer" is focused to determine the feasibility and maximum tolerance dose of Ashwagandha with liposomal doxorubicin (DOXIL) in recurrent ovarian cancer patients. The study contains two parts. In part 1 (phase I), 18 patients with recurrent ovarian cancer eligible for DOXIL therapy will be recruited and three doses of Ashwagandha (2.0 g, 4.0 g and 8.0 g) in the form of tablets along with DOXIL will be evaluated for feasibility and tolerance of ASWD. In part 2 (phase II), 54 patients with recurrent ovarian cancer will be recruited and treated with DOXIL and Ashwagandha (dose determined from part 1) to evaluate the complete response (CR), partial response (PR), and stable disease (SD).

Start Date25 Sep 2024

Sponsor / Collaborator

University of Louisville

[+1]

CTRI/2023/07/055361

/ Not yet recruitingPhase 2IIT

A Phase II Clinical Trial of Standardized Withaferin-A for the treatment of Steroid Refractory acute Graft versus Host Disease.

Start Date31 Jul 2023

Sponsor / Collaborator

Tata Memorial Centre

100 Clinical Results associated with BRMS1

100 Translational Medicine associated with BRMS1

0 Patents (Medical) associated with BRMS1

205

Literatures (Medical) associated with BRMS1

01 May 2025·Molecular Immunology

Estradiol conjugation to estrogen receptorα upregulates Brms1 expression mediating M2 polarization of alveolar macrophages and exacerbating airway inflammation in asthmatic mice

Article

Author: Yan, Jiaqi ; Hua, Mengqing ; Niu, Minzhu ; Chen, Yingzi ; Song, Chuanwang ; Wu, Fan ; Xie, Minyu ; Liu, Xingyue ; Dong, Shu ; Guo, Shujun ; Wu, Wenwen ; Huang, Han ; Li, Ya ; Shang, Feifei ; Du, Yulin

Asthma is a common condition involving chronic airway inflammation that primarily affects women and boys. Estrogen levels correlate with the observed differences in the prevalence of asthma between the sexes, but the exact mechanism is unclear. This study established a castration mice (OVX) model through bilateral ovariectomy surgery, and subcutaneously injected estradiol (E2) into OVX asthmatic mice to analyze the effect of E2 on the onset of asthma. Then, airway inflammation was evaluated in the mice using airway resistance measurements, lung tissue hematoxylin and eosin staining, and eosinophil counts. Furthermore, the proportion of CD206-positive cells and the expression of M2 polarization markers, such as Arg1 and YM1, were detected in alveolar macrophages (AMs). The effects of different concentrations of E2 on M2 polarization of AMs were examined in vitro, and the types of estrogen receptors (ERs) involved were investigated. Transcriptome analysis combined with volcano plots and heatmaps were used to compare the differentially expressed genes to investigate the mechanism by which E2 affects M2 polarization of AMs. The results showed that female asthmatic mice had more severe airway inflammation and higher airway responsiveness than male asthmatic mice. E2 increased airway inflammation and airway resistance in asthmatic mice. E2 not only promoted M2 polarization of AMs in asthmatic mice in vivo, but also increased the expression of M2 markers, such as Arg1 and YM1, by AMs in vitro. The use of ERα antagonist AZD9496 reduced the effect of E2 on the promotion of M2 polarization in AMs. Analysis of transcriptome differences indicated that E2 upregulated expression of M2 breast cancer metastasis suppressor gene 1 (Brms1) in AMs. Notably, antagonism of ERα inhibited this upregulation of Brms1 gene expression. Interference with Brms1 mRNA production reduced the gene expression of Arg1 and YM1 in AMs undergoing M2 polarization after E2 stimulation. In summary, E2 exacerbates airway inflammation in asthmatic mice and binds to ERα, upregulating Brms1 expression and mediating M2 polarization of AMs.

31 Dec 2024·Bioinformation

Molecular docking analysis of pyrrole derivatives with different breast cancer targets

Article

Author: Kulothungan, Vasantha Kumar ; Ilango, Stephen ; K, Girija

Breast Cancer is foremost common type in worldwide and major risk of death in women. SR9009 a pyrrole derivatives and synthetic role of the REV-ERB alpha, core of circadian clock components. Hence it is interest to document the molecular docking analysis of SR9009 with different breast cancer target protein targets such as HER2, Erα, PR, PI3K, AKT, Reverbα, BRMS1, Aromatase and mTOR, CDK4, CDK6, TK and Top II. Among 13 proteins, HER2, Erα, Aromatase, Reverbα, BRMS1 and Top II have good binding score affinity. Molecular Dynamic results show that significant higher binding energy for Reverb alpha + SR9009 complex found to be -220.618 +/- 19.145 kJ/mol compared to Reverb alpha + Doxorubicin complex found to be -154.812 +/- 18.235 kJ/mol. Molecular docking and dynamics analysis show that SR9009 is a potential drug candidate targeting Reverb alpha for anti-breast cancer activity.

01 Oct 2024·Journal of Neuro-Oncology

Exploring the prognostic value of BRMS1 + microglia based on single-cell anoikis regulator patterns in the immunologic microenvironment of GBM

Article

Author: Zhang, Pengpeng ; Wang, Qi ; Xie, Jiaheng ; Cheng, Chao ; Liu, Jinhui ; Ni, Kaixiang ; Zhao, Songyun ; Zhao, Ning ; Liu, Yuankun ; Ji, Wei

AbstractBackgroundAnoikis is a specialized form of programmed cell death induced by the loss of cell adhesion to the extracellular matrix (ECM). Acquisition of anoikis resistance is a significant marker for cancer cell invasion, metastasis, therapy resistance, and recurrence. Although current research has identified multiple factors that regulate anoikis resistance, the pathological mechanisms of anoikis-mediated tumor microenvironment (TME) in glioblastoma (GBM) remain largely unexplored.MethodsUtilizing single-cell RNA sequencing (scRNA-seq) data and employing non-negative matrix factorization (NMF), we identified and characterized TME cell clusters with distinct anoikis-associated gene signatures. Prognostic and therapeutic response analyses were conducted using TCGA and CGGA datasets to assess the clinical significance of different TME cell clusters. The spatial relationship between BRMS1 + microglia and tumor cells was inferred from spatial transcriptome RNA sequencing (stRNA-seq) data. To simulate the tumor immune microenvironment, co-culture experiments were performed with microglia (HMC3) and GBM cells (U118/U251), and microglia were transfected with a BRMS1 overexpression lentivirus. Western blot or ELISA were used to detect BRMS1, M2 macrophage-specific markers, PI3K/AKT signaling proteins, and apoptosis-related proteins. The proliferation and apoptosis capabilities of tumor cells were evaluated using CCK-8, colony formation, and apoptosis assays, while the invasive and migratory abilities of tumor cells were assessed using Transwell assays.ResultsNMF-based analysis successfully identified CD8 + T cell and microglia cell clusters with distinct gene signature characteristics. Trajectory analysis, cell communication, and gene regulatory network analyses collectively indicated that anoikis-mediated TME cell clusters can influence tumor cell development through various mechanisms. Notably, BRMS1 + AP-Mic exhibited an M2 macrophage phenotype and had significant cell communication with malignant cells. Moreover, high expression of BRMS1 + AP-Mic in TCGA and CGGA datasets was associated with poorer survival outcomes, indicating its detrimental impact on immunotherapy. Upregulation of BRMS1 in microglia may lead to M2 macrophage polarization, activate the PI3K/AKT signaling pathway through SPP1/CD44-mediated cell interactions, inhibit tumor cell apoptosis, and promote tumor proliferation and invasion.ConclusionThis pioneering study used NMF-based analysis to reveal the important predictive value of anoikis-regulated TME in GBM for prognosis and immunotherapeutic response. BRMS1 + microglial cells provide a new perspective for a deeper understanding of the immunosuppressive microenvironment of GBM and could serve as a potential therapeutic target in the future.

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BRMS1

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