BCAR3
- Known as:
- BCAR3
- Catalog number:
- 002450A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BCAR3
Related genes to: BCAR3
- Gene:
- BCAR3 NIH gene
- Name:
- BCAR3 adaptor protein, NSP family member
- Previous symbol:
- -
- Synonyms:
- NSP2, SH2D3B, AND-34
- Chromosome:
- 1p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-29
- Date modifiied:
- 2019-01-25
Related products to: BCAR3
Related articles to: BCAR3
- Ferroptosis is an iron-dependent programmed cell death, which plays a complex role in pancreatic ductal adenocarcinoma (PDAC), regulating both tumor development and immune interaction. However, the clinical significance and potential molecular mechanism of ferroptosis in PDAC have not been fully clarified, which limits its application in treatment. - Source: PubMed
Publication date: 2026/07/13
Liu WeiShen YifenRao LiQiao ZhenguoLing XinCheng LongShen Genhai - Observational studies on sex hormones and oral cavity cancer show inconsistent results. This two-sample Mendelian randomization (MR) study investigated potential causal associations between genetically predicted levels of six key sex hormone-related factors - total testosterone (TT), sex hormone-binding globulin (SHBG), estradiol (E2), estrogen receptor (ESR), estrogen sulfotransferase (EST), and breast cancer anti-estrogen resistance protein 3 (BCAR3) - and oral cavity cancer risk. - Source: PubMed
Publication date: 2025/06/22
Qu XiaopengTao PengyuDong JiajiaMeng Lingzhao - Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic treatments. This study evaluates the anticancer activity and mode of action of the copper(II) complex [Cu(HL)(NO)HO]·HO (CuHL), derived from (E)-N'-(2-hydroxy-3-methoxybenzylidene)furan-2-carbohydrazide (HL), against a panel of TNBC cell lines (MDA-MB-231, MDA-MB-468, MDA-MB-157, HCC1806). CuHL exhibits potent cytotoxicity in the low micromolar range (IC ≈ 2 µM), surpassing cisplatin by up to 81-fold. In MDA-MB-231 cells, CuHL inhibits colony formation and induced reactive oxygen species (ROS) generation in a concentration-dependent manner. Moreover, CuHL triggers apoptosis as evidenced by Annexin V/PI staining and the modulation of Bax, Bcl-2, caspase-3, and cleaved caspase-3 protein levels. Label-free quantitative proteomics reveal 34 differentially expressed proteins, implicating pathways related to heat shock response, protein folding, lipid metabolism, and cell migration. Notably, CuHL downregulates BCAR3, AJUBA, MPZL1, TP53, FASN, and HMGCS1, suggesting inhibition of prometastatic and lipid biosynthetic processes. Functional assays confirm reduced migratory capacity in MDA-MB-231 cells. These findings position CuHL as a promising candidate for TNBC therapy, meriting further in vivo evaluation. - Source: PubMed
Santa Maria de la Parra LucíaMartínez Valeria RNayeem NaziaContel MariaLeón Ignacio E - Around 30% of patients with hormone receptor-positive (HR+) breast cancer acquire resistance to endocrine therapy combined with cyclin-dependent kinase 4/6 inhibitors (CDK4/6i), which are first-line treatments in metastatic settings. Therefore, we aimed to identify loci associated with resistance to endocrine therapy and CDK4/6i; this was achieved using retroviral vectors, which randomly insert gene-disrupting elements into the genome, causing gene expression alterations and potentially leading to therapy resistance. ER-positive ZR75.1 breast cancer cells transduced with retroviral vectors were treated with endocrine (tamoxifen, fulvestrant) or CDK4/6i monotherapies (abemaciclib, palbociclib, ribociclib) or a combination of fulvestrant and ribociclib. DNA was extracted, and virus integration sites (VISs) were characterized according to the detection frequency and read depth using next-generation sequencing (VIS-NGS). Resistance-associated VIS loci were identified when differentially presented in treated samples compared to controls. Well-established tamoxifen resistance genes (, , ) were detected, enabling the validation of our approach. Thirty-seven VIS loci were associated with resistance to fulvestrant and ribociclib monotherapies. Twenty of these loci were also identified as candidates for resistance to other CDK4/6i and to fulvestrant and ribociclib combination therapy, including and -genes that are involved in resistance to endocrine therapy but have not yet been associated with resistance to CDK4/6i. The identification of unique and shared resistance-associated loci highlights the complexity of resistance pathways. - Source: PubMed
Publication date: 2026/01/29
Huang ZhangzanBeaufort CorineHelmijr JeanZantboer BrianRozema GiadaMuritti CamillaWhien Julia JUijterwegen AnnaMassimino MicheleMartens John W MJansen Maurice P H M - has been implicated in various cancers, yet its role in thyroid cancer (TC) remains unclear. This study aimed to investigate the methylation status, functional effects, and underlying mechanisms of in TC. - Source: PubMed
Publication date: 2026/01/15
Yu WenkangMao YizhuYin YifeiYang JiachengZhang YiHuang XuandongZhang YifenJiang ChenxiaYang Rongxi