Ask about this productRelated genes to: SURF6 Blocking Peptide
- Gene:
- SURF6 NIH gene
- Name:
- surfeit 6
- Previous symbol:
- -
- Synonyms:
- FLJ30322, RRP14
- Chromosome:
- 9q34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2016-10-05
Related products to: SURF6 Blocking Peptide
Related articles to: SURF6 Blocking Peptide
- Prostate cancer (PCa) remains a major health challenge globally, necessitating the identification of novel therapeutic targets to improve patient outcomes. This study investigates the role of the SURF6 gene in PCa, focusing on its expression patterns, molecular mechanisms, and biological behaviours in vitro and in vivo. We employed a combination of bioinformatics analysis, gene expression profiling, Western blotting, and functional assays, including cell proliferation, migration, invasion, and stemness assays, to evaluate the impact of SURF6 modulation in PCa cell lines. Our findings demonstrate that SURF6 is significantly upregulated in PCa tissues compared to adjacent normal tissues, with elevated expression correlating with poor prognosis and advanced clinical stages. Functional assays revealed that silencing SURF6 inhibited PCa cell proliferation, migration, and invasion, while overexpression of SURF6 enhanced these malignant characteristics. Notably, we identified that SURF6 regulates CDK4 expression, which plays a pivotal role in cell cycle progression and maintenance of stem-like properties, as evidenced by the modulation of cancer stem cell markers such as CD44 and Nanog. Furthermore, we elucidated that METTL3 and YTHDF1 regulate SURF6 expression through mA modification. In vivo experiments confirmed that knockdown of SURF6 inhibits tumour growth and reduces stemness features in xenograft models. Overall, our study underscores the critical role of SURF6 in promoting PCa progression and highlights its potential as a therapeutic target, paving the way for future research focused on targeting SURF6 in clinical settings to improve treatment strategies for PCa. - Source: PubMed
Cheng YueZhang MinShi DanfangXia XuFen - The causal relationship between gut microbiota (GM) and white matter injury and communication remains unclear. We aimed to scrutinize the plausible causal impact of GM on white matter hyperintensities (WMHs), white matter microstructure, white matter connectivity, and multiple neurological diseases via Mendelian randomization study. We identified four WMH-related bacterial taxa, including class , order , family , and genus In addition, three bacterial taxa were discovered that have consistent effect on multiple aspects of white matter microstructure. Furthermore, we found 12 strong associations between genetic liability in GM and white matter connectivity. Among these bacterial taxa, the family demonstrated a protective effect against ischemic stroke (IS). The genus showed protective effect on IS and small vessel stroke while posed a risk effect on neuromyelitis optica spectrum disorder (NMOSD), as well as on aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (AQP4-IgG+ NMOSD). The order and family showed protective effect against cardioembolic stroke, and the genus showed a protective effect on amyotrophic lateral sclerosis. In terms of the mapped genes of statistically significant bacterial taxa, genes such as , , , , , and exhibited a significant causal correlation with the corresponding white matter connectivity. This study demonstrated a genetically predicted causal relationship between GM and WMH, white matter microstructure, white matter connectivity, and multiple neurological diseases, based on GWAS data from mixed-sex cohorts without sex-stratified summary statistics. These findings highlight the potential role of GM in influencing brain structural integrity. - Source: PubMed
Publication date: 2025/09/04
Zhang LanPang Xiao-WeiZhang Lu-YangZhu Li-FangLi Wan-NingChu Yun-HuiZhou Luo-QiTian Dai-ShiQin ChuanChen Lian - The hierarchical, multiphase organization of the nucleolus underlies ribosome biogenesis. Ribonucleoprotein particles that regulate ribosomal subunit assembly are heterogeneously disposed in the granular component (GC) of the nucleolus. However, the molecular origins of the GC's spatial heterogeneity and its association with ribosomal subunit assembly remain poorly understood. Here, using super-resolution microscopy, we uncover that key GC biomolecules, including nucleophosmin (NPM1), surfeit locus protein 6 (SURF6), and ribosomal RNA (rRNA), are heterogeneously localized within sub-phases in the GC. In vitro reconstitution showed that these GC biomolecules form multiphase condensates with SURF6/rRNA-rich core and NPM1-rich shell, providing a mechanistic basis for GC's spatial heterogeneity. SURF6's association with rRNA is weakened upon ribosome subunit assembly, enabling NPM1 to extract assembled subunits from condensates-suggesting an assembly-line-like mechanism of subunit efflux from the GC. Our results establish a framework for understanding the heterogeneous structure of the GC and reveal how its distinct sub-phases facilitate ribosome subunit assembly. - Source: PubMed
Publication date: 2025/03/04
Dogra PriyankaFerrolino Mylene CKhatun SuparnaTolbert MicheleMiao QiPruett-Miller Shondra MPitre AaronTripathi SwarnenduCampbell George EBajpai RichaFreyaldenhoven TolerGibbs EricPark Cheon-GilKriwacki Richard W - This study aims to investigate the role of cuprotosis in fluorosis and identify potential targeted drugs for its treatment. The GSE70719 and GSE195920 datasets were merged using the inSilicoMerging package. DEGs between the exposure and control groups were found using R software. Overlapping genes of DEG and cuprotosis-related genes (CRGs) were obtained by Venn diagram and were enriched by GO and KEGG. Hub genes were identified using PPI networks and enriched by GSEA. ROC curves, the xCell algorithm, and consensus cluster analysis were utilized to evaluate diagnostic efficacy, examine immune cell infiltration, and identify cuproptosis subtypes, respectively. The GSE53937 dataset was used for external validation. The DSigDB database was used to predict small molecule drugs. Molecular docking was used to validate the relationship between small molecule drugs and hub genes. A total of 1522 DEGs (743 upregulated genes and 779 downregulated genes) and 33 overlapping genes of DEGs and CRGs were obtained. The 33 overlapping genes were enriched in ribosomal biogenesis and oxidative phosphorylation pathways. The hub genes DNTTIP2, GTPBP4, IMP4, MRPL12, MRPL13, MRPL2, MRPS2, MRPS22, NOP2, RSL1D1, and SURF6 were identified, demonstrating great diagnostic ability with AUC > 0.8. These hub genes were associated with immune response and inflammation. Two cuproptosis patterns were established based on 33 CRGs. Mepacrine was screened as a potential drug and demonstrated stability in docking with IMP4. In summary, the current study identified several CRGs that may serve as potential biomarkers for diagnosing fluorosis and are involved in fluoride-induced immune responses. Additionally, mepacrine was screened as a potential treatment for fluorosis by targeting CRGs. - Source: PubMed
Publication date: 2025/01/21
Ba RuijieLiu BinFeng ZichenWang GuoqingNiu ShuWang YanJiao XuechengWu CuipingYu FangfangZhou GuoyuBa Yue - KRAS mutations are associated with poor prognosis in colorectal cancer (CRC). Although the association between the gut microbiota and CRC has been extensively documented, it is unclear whether KRAS mutations can regulate the gut microbiota. Metagenomics has identified changes in the diversity of the gut microbiota in CRC due to KRAS mutations. Specifically, KRAS mutations positively correlate with the abundance of the bacteroides. Understanding how to regulate the classic carcinogenic bacterium within the bacteroides, such as enterotoxigenic bacteroides fragilis (ETBF), to enhance treatment efficacy of tumors is a key focus of research. Mechanistically, we found that the reduction of miR3655 is indispensable for KRAS mutation-promoted proliferation of CRC and the abundance of ETBF. miR3655 targets SURF6 to inhibit its transcription. Further transcriptomic sequencing revealed that SURF6 promotes intratumoral colonization of ETBF in CRC by inhibiting the nuclear translocation and transcription levels of the IRF7, affecting the activation of the IFNβ promoter. Regulating miR3655 and SURF6 can promote IFNβ secretion in CRC, directly killing ETBF. These data indicate that KRAS mutations affect the intratumoral colonization of ETBF in CRC through the miR3655/SURF6/IRF7/IFNβ axis. This provides new potential strategies for treating CRC associated with KRAS mutations or high levels of ETBF. - Source: PubMed
Publication date: 2024/11/10
Chen YizhenLiu ShaolinTan SongZheng YuanyuanChen YifanYang ChangshunLin ShengtaoMi YulongLi Weihua