Rabbit Anti-Human BRMS1 (a.a. 151-246) Polyclonal antibody

Background: Breast cancer metastasis suppressor 1 (BRMS1) is a potent metastasis suppressor of various types of malignancies, including melanoma and ovarian cancer. Unfortunately, the clinical data regarding its role as a true metastatic suppressor and its efficacy as a prognostic marker and therapeutic target remain controversial. This study was designed to investigate the effect of BRMS1 on the invasion and metastasis of human ovarian cancer cells and its potential underlying mechanisms. Materials and Methods: BRMS1 small interfering RNAs (siRNAs) or control siRNAs were transfected into the OVCAR3 human ovarian cancer cell line. Invasion and migration activities were assessed using the Transwell invasion and migration assay. Protein levels of nuclear factor-kappa B (NF-kappa B) subunit p65, osteopontin (OPN) and urokinase-type plasminogen activator (uPA) were evaluated by Western blot, immunofluorescence and immunocytochemistry methods. Results: Successful knockdown of BRMS1 was verified by quantitative real-time RT-PCR and Western blot. The invasion and migration capacities of OVCAR3 cells were significantly enhanced in the BRMS1-silenced group, compared to controls (p < 0.05). Silencing of BRMS1 significantly induced the expression of NF-kappa B subunit, p65, uPA, and OPN proteins. Conclusions: BRMS1 inhibits expression of p65, uPA and OPN protein. In turn, this leads to inhibition of ovarian cancer cell invasion and metastasis. This study unveils a potential novel mechanism by which BRMS1 inhibits metastasis of ovarian cancer cells.

Cancer research studies using next-generation sequencing have revealed a number of genes of which aberrant expression is associated with various cancers. Recently, long non-coding RNA (lncRNA) has been highlighted due to its tissue-specific expression and cell cancerization functions, such as the regulation of key tumor suppressors. In this study, we suggest a very efficient approach to survey lncRNAs putatively associated with breast cancer. We targeted lncRNAs linked with breast cancer associated genes (BCAGs) and analyzed their expression pattern in human breast cancer cell lines. A total of 337 BCAGs were retrieved from literature review and the existence of 121 lncRNAs were identified from the 15 kb up- and downstream regions of the list of genes. Twenty lncRNAs' expression were detectable in human breast cancer cell lines with different expression patterns. Interestingly, the expression of three lncRNAs, two up-regulated (RAD51C v.4, LOC105371849) and one down-regulated (LOC102724064), were closely correlated with adjacent BCAGs (RAD51C, HEATR6 and BRMS1) in breast cancer cell lines. We thus demonstrated association between the lncRNA and its adjacent BCAG using LOC105371849-HEATR6, of which the function and regulation in breast cancer are still unknown. Knockdown of LOC105371849 by siRNA decreased the expression of HEATR6 mRNA in the MCF7 human breast cancer cell line. In conclusion, this study provides a better understanding about the biological roles of lncRNAs in breast cancer and may be useful in the investigation of proper targets for diagnostic and/or therapeutic breast cancer markers using public databases.