Ask about this productRelated genes to: RAB25 Blocking Peptide
- Gene:
- RAB25 NIH gene
- Name:
- RAB25, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- CATX-8
- Chromosome:
- 1q22
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-18
- Date modifiied:
- 2014-11-19
Related products to: RAB25 Blocking Peptide
Related articles to: RAB25 Blocking Peptide
- CEU-938, an innovative antimicrotubule prodrug bioactivated by cytochrome P450 1A1 (CYP1A1), represents a promising targeted alternative for cancer cells overexpressing this enzyme. To optimize its clinical utility and minimize off-target effects in breast cancer (BC) patients, this study aims to identify predictive biomarkers of CEU-938 efficacy. The antiproliferative activity of CEU-938 was assessed across a panel of 39 human breast cancer and non-tumorigenic cell lines. Differential expression analyses were subsequently performed to distinguish CEU-938-responsive from non-responsive cell lines using a threshold of 1000 nM. Candidate biomarkers identified through this approach were then validated by RT-qPCR and Western blot analyses. CEU-938 demonstrated marked and selective antiproliferative activity across molecular subtypes of human breast cancer, with efficacy observed in approximately 40% of triple-negative breast cancer (TNBC), 70% of estrogen receptor-positive (ER), and 80% of human epidermal growth factor receptor 2-positive (HER2) breast cancer cell lines, while sparing non-tumorigenic human breast cells (MCF 10A, MCF-12A, 184B5). Differential expression analysis identified five candidate biomarkers associated with CEU-938 responsiveness, namely, FOXA1 (log2-fold change (LFC) = 3.1), RAB25 (LFC = 3.8), RHOV (LFC = 2.9), PRKCH (LFC = 1.6), and HDAC9 (LFC = -1.7). Among these, FOXA1 and RAB25 robustly validated by RT-qPCR and Western blot analyses, showing strong inverse correlations with CEU-938 sensitivity (Spearman correlation coefficients of -0.82 and -0.61, respectively, at the protein level). The predictive value of FOXA1 and RAB25 was further confirmed by Western blot analyses in two independent breast cell line models, the non-responsive MCF-12A and the responsive MDA-kb2. Collectively, these findings identify FOXA1 and RAB25 as robust predictive biomarkers of response to CEU-938. Notably, FOXA1 and RAB25 are strongly implicated in breast cancer biology, and FOXA1 has been directly linked to the aryl hydrocarbon receptor (AHR), the main regulator of CYP1A1. These results position CEU-938 as a strong precision-therapy candidate that combines target selectivity, a favorable toxicity profile, and biomarker-enabled patient stratification, with potential clinical benefit in ER and HER2 enriched tumors, as well as a subset of TNBC. - Source: PubMed
Publication date: 2026/02/25
Bruxelles QuentinHamel-Côté GenevièveScott-Boyer Marie-PierOuellette VincentC-Gaudreault RenéDurocher FrancineDiorio CarolineDroit ArnaudFortin Sébastien - Despite the clinical possibility of reducing hepatitis B virus (HBV) to almost undetectable levels through nucleotide analogs or interferon, the process of hepatic fibrosis in HBV hepatitis carriers perdures. This study will investigate the function of RAB25 in HBV-induced liver fibrosis and related mechanisms. In the study, the expression level of RAB25 was shown to be increased within liver fibrotic tissue samples in Gene Expression Omnibus (GEO) microarrays (GSE171294 and GSE84044) and clinical samples as well as in HBV-induced hepatic stellate cells (HSCs) activation. Silencing RAB25 inhibited HSCs activation induced by TGF-β1 and HBV-associated hepatocellular carcinoma cells HepG2.2.15, also significantly inhibited HSCs viability, proliferation, and migration and the expression levels of α-SMA, Collagen I, MMP2, and PCNA. However, the overexpression of RAB25 significantly promoted HBV-associated hepatocellular carcinoma cells and TGF-β1-induced HSCs activation. Mechanistically, silencing RAB25 in HSCs significantly repressed PI3K/AKT activation triggered by HBV-associated hepatocellular carcinoma cells. However, the overexpression of RAB25 notably promoted PI3K/AKT activation. In conclusion, silencing of RAB25 inhibits HBV-associated hepatocellular carcinoma cell-induced hepatic fibrosis by suppressing the PI3K/AKT signaling. RAB25 has been proven to be an underlying target for clinical treatment of HBV-associated liver fibrosis. - Source: PubMed
Publication date: 2026/02/04
Liu JingLiu BingjieXie XiaYang XinLiu Qiong - Ethylene oxide (E.O) is an ether compound that negatively affects male reproduction, specifically by impairing sperm function. However, the molecular mechanisms underlying the E.O-induced inhibition of sperm function remain poorly understood. Therefore, this study investigated the molecular mechanisms behind E.O-induced toxic effects on sperm motility by assessing Ras-associated binding (Rab) proteins. Therefore, 31 individual Duroc semen samples were analyzed to determine the correlations between Rab protein (Rab3A, Rab5, Rab14, Rab25, Rab27A, and Rab34) levels and sperm motility after exposure to 100-μM E.O. The results showed that E.O exposure significantly reduced sperm motility and motion kinematics. Furthermore, correlation analysis revealed that, in the control group, Rab3A, Rab5, Rab14, Rab25, Rab27A, and Rab34 levels were correlated with various sperm motion parameters. In contrast, only Rab3A and Rab14 levels correlated with multiple sperm motility and kinematic parameters in the 100-μM-E.O group. These results suggest that E.O may affect sperm motion parameters via the action of Rab proteins, leading to decreased sperm motility. Consequently, these findings provide important evidence of the molecular mechanisms underlying E.O-induced toxic effects on sperm function. - Source: PubMed
Publication date: 2026/01/12
Jo Jae-HwanClaudine UwamahoroJang Seung-IkJung Eun-JuLee Woo-JinBae Jeong-WonKim DaehyunMoon JoonhoNam Seung WonChung Eu JinYi JunkooKwon Woo-Sung - - Source: PubMed
Publication date: 2026/01/09
Park Seol HeeSeo Wonhyo - - Source: PubMed
Publication date: 2026/01/06
Zhan Zi-BinLiu Xue-WenLi Ze-HuaZeng Fan-HongBai Kun-HaoWeng Jun