Ask about this productRelated genes to: BRMS1L Blocking Peptide
- Gene:
- BRMS1L NIH gene
- Name:
- BRMS1 like transcriptional repressor
- Previous symbol:
- BRMS1
- Synonyms:
- MGC11296, FLJ39177
- Chromosome:
- 14q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-05
- Date modifiied:
- 2018-05-04
Related products to: BRMS1L Blocking Peptide
Related articles to: BRMS1L Blocking Peptide
- This study aims to investigate the effects of miR-4775 on pancreatic cancer cell (PC) invasion and migration, and to elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/01/05
Song YaxiHan BingLiu QianliFan RuiYang Xiao - Chemoresistance remains a crucial obstacle in breast cancer therapy. The mechanisms underlying chemoresistance need to be explored urgently and in depth. Breast cancer metastasis suppressor 1 like (BRMS1L), a core component of the Sin3A-histone deacetylase (HDAC) co-repressor complex, has been reported to suppress breast cancer metastasis through epigenetically regulating the Wnt signal pathway. However, whether BRMS1L could regulate chemosensitivity has not been explored. Herein, we found that higher BRMS1L expression was significantly correlated with increased chemotherapy sensitivity and better prognosis in patients receiving neoadjuvant chemotherapy. experiments confirmed that chemoresistant breast cancer cells exhibited decreased BRMS1L expression compared to chemosensitive cells. experiments in nude mice demonstrated that BRMS1L markedly strengthened the chemotherapy effects on xenografts. RNA sequencing (RNA-seq) was performed to elucidate the molecular mechanism underlying BRMS1L-mediated chemosensitivity. Bioinformatics analysis indicated that BRMS1L promotes chemotherapy sensitivity by regulating cellular autophagy. Furthermore, chemoresistant breast cancer cells exhibited elevated autophagy levels, and ectopic expression of BRMS1L significantly suppressed protective autophagy through downregulating ATG5. Collectively, these results revealed that BRMS1L enhances chemotherapy sensitivity via inhibiting protective autophagy. To our knowledge, this is the first study that showed that reduced BRMS1L expression is associated with poor response to neoadjuvant chemotherapy and unfavorable prognosis in breast cancer patients. Our findings reveal a novel role of BRMS1L in chemosensitivity and highlight its potential clinical application in the treatment of breast cancer. - Source: PubMed
Publication date: 2025/11/07
Li YuanZhang DianZhao JunhaoYang MeiWang YipingLee PeiyaoQu Shaohua - Renal cancer is among the deadliest human malignancies. MCM7, a cell cycle-regulating protein, is frequently overexpressed in cancers and is associated with hyperproliferation and cancer progression. miR-25-3p, miR-93-5p, and miR-106b-5p form the miR-106b-25 cluster, located within the gene, and have previously been reported as upregulated in RCC. This study investigates whether miRNAs from the miR-106b-25 cluster regulate common target genes, enhance one another's effect, and act synergistically with MCM7 to promote tumor progression. Tissue samples from clear cell RCC (ccRCC) and paired controls were analysed to assess MCM7 expression and genes targeted by the miR-106b-25 cluster. Findings were further validated using the TCGA-KIRC dataset. Functional studies in RCC-derived cell lines were conducted to evaluate the effects of miRNAs on target gene expression, as well as MCM7, and the combined contributions of MCM7 and the miR-106b-25 cluster to renal cancer progression. We demonstrate that MCM7 is upregulated at both transcript and protein levels in RCC, contributing to cancer progression by regulating cell proliferation and caspase-3/7 activity. Furthermore, we identified cancer-related genes aberrantly expressed in ccRCC (, , , , , , ) and targeted by members of the miR-106b-25 cluster, suggesting that their dysregulation may be driven by these miRNAs. Inhibition of the miR-106b-25 cluster increases caspase-3/7 activity. These findings demonstrate that both MCM7 and the miR-106b-25 cluster contribute to renal cancer progression. - Source: PubMed
Publication date: 2025/09/04
Głuchowska Katarzyna MHofman Bartłomiej - 2,3,7,8-Tetrachlorodibenzo--dioxin (TCDD) is a toxic compound affecting organs like the liver, kidney, lung, and reproductive systems in mammals. This study outlines a strategy for choosing appropriate HKGs for tissue-specific gene expression analysis in TCDD toxicity, including four steps: i) identifying candidate HKGs from literature and databases; ii) defining primers from literature or designing new ones; iii) validating primer efficiency and specificity; iv) experimentally assessing candidate HKGs' stability in various tissues of TCDD-exposed mice. Based on this strategy, a total of 40 potential HKGs was selected, further filtered based on their database sources and ranked according to their frequency of use or expression stability. Ultimately, we identified a final set of 15 HKGs (, , , , , , , , , , , , , and ) with typical efficiencies for further evaluation. Then, the stability of the selected HKGs was determined in the liver, kidney, lung, ovary and testis of TCDD-exposed mouse compared to the control group using the [log (2)] and statistically analyzed using Pearson correlation coefficient () by BestKeeper algorithm. Our data analysis revealed that , , and were the most stable HKGs for normalizing gene expression in the liver, while , , and were suitable for kidney tissue. In the lung, , , and showed stability, while , , and were most stable in ovary. Lastly, , , and were accurately stable in the testis of TCDD-exposed mice. Our study identifies stable HKGs, improving TCDD toxicity research accuracy and reliability. - Source: PubMed
Publication date: 2025/04/27
Hammoudeh NourHasan ReemDeeb MohammadRadwan ZuherAyoubi OmarAlendary RoaaYoussef MouayadKazan AbdulfattahAlsahli RasilFaiad WalaaAldeli NourHanano Abdulsamie - Low expression levels of breast cancer metastasis suppressor 1 like (BRMS1L) have been associated with the growth of cancer cells. However, the mechanisms underlying the role of BRMS1L as an antitumour transcription factor in the progression of NSCLC have not been explored. Herein, we reveal that BRMS1L plays a key role as a tumour suppressor in inhibiting NSCLC proliferation and metastasis. Mechanistically, BRMS1L overexpression results in the downregulation of glutathione peroxidase 2 (GPX2) expression and consequently causes abnormal glutathione metabolism and increased levels of reactive oxygen species (ROS) in cells, inducing oxidative stress injury and apoptosis. Furthermore, overexpression of GPX2 enhances the growth advantage and oxidative stress repair conferred by knockdown of BRMS1L. Importantly, we show that low expression of BRMS1L in NSCLC cells causes relatively high levels of antioxidant accumulation to maintain cell redox balance and renders cancer cells more sensitive to treatment with piperlongumine as an ROS inducer both in vitro and in vivo. These findings offer new insights into the role of BRMS1L as a transcriptional repressor in NSCLC and suggest that the BRMS1L expression level may be a potential biomarker for predicting the therapeutic response to small molecule ROS inducers, providing new ideas for targeted therapy. - Source: PubMed
Publication date: 2024/01/22
Cao PenglongGu JuebinLiu MulinWang YingxinChen MingyingJiang YizhuWang XiaoyanZhu SiqiGao XueLi Shijun