Ask about this productRelated genes to: WNT7B Blocking Peptide
- Gene:
- WNT7B NIH gene
- Name:
- Wnt family member 7B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-10-05
Related products to: WNT7B Blocking Peptide
Related articles to: WNT7B Blocking Peptide
- We investigated the potential of miR-640 to downregulate CDK4/6 inhibitor resistance-associated genes and evaluated its apoptotic, anti-metastatic and anti-proliferative effects, both alone and in combination with abemaciclib in breast cancer cells. miR-640 was identified via GSE126125 dataset analysis. Targets were predicted using miRDB, TargetScan and TargetMiner, filtering for resistance-associated genes. MTT assays determined IC50 values for abemaciclib and combinations. Functional effects were evaluated in MCF7 and MDA-MB-231 cells through Annexin V, cell cycle and wound healing assays. Target gene expression was quantified by RT-qPCR. Successful transfection significantly upregulated miR-640 (~50-fold). The miR-640/abemaciclib combination strongly inhibited migration, induced apoptosis and triggered cell line-specific phase arrests (S and G2/M in MCF7; G0/G1 in MDA-MB-231). Gene expression analysis showed significant downregulation of a comprehensive resistance network (including CDK4/6, CDKN2B, WNT7B, MAP3K1 and AURKA) in MCF7 cells. In MDA-MB-231 cells, PDK1, CDK6, CDKN2B, SMAD2, ZFP91, MAP3K1 and AURKA were significantly suppressed. This study identifies miR-640 as a potent tumour suppressor that resensitises breast cancer cells to CDK4/6 inhibition. By post-transcriptionally downregulating key resistance genes, miR-640-alone or additively with abemaciclib-suppresses proliferation and migration while inducing apoptosis, emerging as a promising combinatorial therapeutic strategy. - Source: PubMed
Alkac Ismail MertBiray Avci Cigir - - Source: PubMed
Sun Wei-LiKang TianWang Yuan-YuSun Jian-PingLi ChenLiu Hong-JiangYang YueJiao Bao-Hua - This study aimed to investigate the therapeutic effect of Huangqin Qingre Chubi Capsules(HQC) on rheumatoid arthritis(RA) and the mechanism of inhibiting RA macrophage polarization by reducing the entry of intestine-derived lipopolysaccharide(LPS) into the bloodstream. ELISA and 16S rRNA analysis were used to assess the inhibitory effect of HQC on LPS in the intestinal contents of mice in vivo. The effect of HQC on macrophage proliferation was detected by CCK-8 assay to determine the appropriate dose of drug-containing serum. RT-qPCR and immunofluorescence assay were used to detect the expression of genes related to macrophage polarization. Transcriptomics was used to predict the biomolecular function of macrophages upon LPS stimulation, and molecular docking was utilized to verify the binding of key HQC components to Wnt family member 7b(Wnt7b). Following co-culture of macrophages with fibroblast-like synoviocytes(FLS), RT-qPCR, Western blot, scratch assay, flow cytometry, and immunofluorescence assay were employed to investigate the regulatory mechanism of HQC on M1 macrophage-FLS communication via the Wnt/β-catenin signaling pathway. The results showed that LPS was highly expressed in the intestinal contents of collagen-induced arthritis(CIA) model mice, and HQC administration exhibited a negative correlation with this expression. M1 macrophages promoted the expression of inflammatory factors such as inducible nitric oxide synthase(iNOS), tumor necrosis factor-α(TNF-α), and interleukin-6(IL-6), and also increased oxidative activity; these effects could be reversed by HQC. Transcriptomic analysis predicted that the Wnt/β-catenin signaling pathway was highly correlated with the effect of HQC on macrophage polarization in RA treatment. HQC-containing serum inhibited FLS migration, promoted apoptosis, and suppressed the expression of key genes in the Wnt signaling pathway, including c-Myc, CCND1, and β-catenin. Molecular docking indicated strong binding affinity between key components of HQC and Wnt7b. Overexpression of Wnt7b in macrophages, followed by co-culture with FLS, significantly interfered with the therapeutic effects of HQC. These findings demonstrated that HQC alleviates RA by inhibiting the entry of intestine-derived LPS into the bloodstream, thereby blocking M1 macrophages-FLS communication. - Source: PubMed
Wang BingChen Jia-QingPulati ZiyadanZheng Liang-ChenHu MinXia Ai-XinLi Yan-PingXu Wen-BoMiao Cheng-Gui - Urinary tract infections (UTIs) are among the most common bacterial infections, yet the genetic factors influencing susceptibility remain poorly understood. We performed a genome-wide association study of recurrent UTI involving 1,860,836 individuals (213,869 cases and 1,646,967 controls). We identified 36 independent non-HLA genome-wide significant loci encoding kidney epithelial and immune response genes and demonstrated that some loci have sex-specific effects. Integrative functional annotation, expression and protein quantitative trait locus colocalization, and single-cell multi-omic analyses revealed that UTI risk alleles preferentially modulated gene expression in kidney, ureter, and bladder epithelia. Multi-omic prioritization converged on a number of pathogenic pathways: epithelial barrier and mucosal glycocalyx defense (, , , ), innate immune regulation (, , ), infection resolution and regulated cell death (, , ), epithelial identity maintenance (, , ), urinary tract development (, , , , ), and nutritional immunity through iron sequestration (). Approximately one-third of loci colocalized with gene expression in kidney tubules, suggesting direct modulation of epithelial host-defense programs. Among all loci, , which encodes a GPI-anchored epithelial surface protein expressed in the kidney papilla and urinary tract epithelia, emerged as the strongest candidate causal gene. We demonstrated that PSCA was secreted into urine, bound uropathogenic , and inhibited bacterial growth , implicating it as a constitutive epithelial defense factor. We also demonstrated that while was protective against urinary infections and duodenal ulcers, it was associated with increased risk of bladder, prostate, and gastric cancers, suggesting antagonistic pleiotropy between mucosal defenses and oncogenesis. Together, our findings define the polygenic architecture of UTI susceptibility, highlighting epithelial surface defense, innate immune regulation, developmental patterning, and nutritional immunity as central components of host defense, providing a new framework for host-directed, non-antibiotic interventions. - Source: PubMed
Publication date: 2026/07/10
Xu KatherineKhan AtlasShang NingZeng WenjieWang ChenBerrouet CeciliaShen Tian HuaiNarayanan PadmaDeng JennyDiPerna ChiaraWilliams CharlotteCuacuas SarahOlsen Timothy RArace JeffreyGhotra AryanMonical WayneBorisov OlegHaug StefanLiu HongboHa EunjiBanlengchit RunLevitman AbrahamPatel DiyaChou ClaireHalibart BartlomiejGuo Tai WeiSimmons ShawnGoswami SanyaNesanir KivancFujita MasashiKullo Iftikhar JJarvik Gail PWei Wei-QiFeng QiPingJiang LanStein C MichaelWeng ChunhuaHripscak GeorgeGharavi Ali GSusztak KatalinDe Jager Philip LKöttgen AnnaBarasch JonathanSims Peter AKiryluk Krzysztof - Endocrine therapy (ET) selection in estrogen receptor-positive breast cancer (ER + BC) is guided by menopausal status and tolerability rather than tumor biology, despite substantial heterogeneity in recurrence. We hypothesized that baseline gene expression differentially associates with recurrence depending on initial ET class. In a retrospective cohort of 74 ER+/HER2- patients treated with adjuvant ET, we profiled baseline tumor RNA and fitted adjusted Cox models for gene and ET interactions on time-to-recurrence and time-to-switch. Among selective estrogen receptor modulators-initiated patients, higher expression of , , , , and was associated with markedly increased recurrence, while no comparable association was observed among aromatase inhibitors-initiated patients. Forty-one percent of patients switched ET at least once, predominantly due to intolerance (joint pain, unspecified side effects); switching was not consistently associated with tumor biology. These hypothesis-generating findings identify candidate gene and ET interactions and motivate validation in larger, independent cohorts. - Source: PubMed
Publication date: 2026/06/30
Jones VeronicaWang YongzheQuinones ChristineAljaber DanaNelson EvaNath AritroKang IreneRugo HopeYee LisaSeewaldt VictoriaMortimer Joanne