Ask about this productRelated genes to: Twist1 antibody
- Gene:
- TWIST1 NIH gene
- Name:
- twist family bHLH transcription factor 1
- Previous symbol:
- ACS3, BPES3, TWIST, CRS
- Synonyms:
- SCS, H-twist, BPES2, bHLHa38, CRS1
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-10-05
Related products to: Twist1 antibody
Related articles to: Twist1 antibody
- - Source: PubMed
Tao YoumaoHan TaoZhang TaoMa ChongSun Caixia - Metastasis remains a major therapeutic challenge in hepatocellular carcinoma (HCC), yet its underlying molecular mechanisms are not fully understood. This study reveals that ZCCHC4 acts as a key promoter of HCC metastasis. We demonstrate that ZCCHC4 enhances the metastatic capacity of HCC cells both and . Mechanistically, ZCCHC4 upregulates key lipid biosynthesis enzymes (HMGCR, SQLE, FASN, and SCD), leading to intracellular accumulation of cholesterol and fatty acids which drive metastasis. Concurrently, ZCCHC4 transcriptionally activates TMEM97, thereby augmenting Wnt signaling. Furthermore, TMEM97 interacts with LCN2 to retain it in the cytoplasm. This sequestration relieves LCN2-mediated inhibition of the transcription factor Twist1, consequently promoting epithelial-mesenchymal transition (EMT) and metastasis. Consistent with these findings, ZCCHC4 level positively correlates with levels of TMEM97 and the lipid enzymes in clinical HCC specimens, and high ZCCHC4 expression is associated with poor patient prognosis. In summary, our work identifies ZCCHC4 as a critical metastasis driver via coordinated regulation of lipid metabolism and the TMEM97/LCN2/Twist1 axis, presenting novel potential targets for treating HCC metastasis. - Source: PubMed
Publication date: 2026/03/25
Ye JuanWen XinyiLiu RuiyangHuang CainiXu ZhijieZhan YiXu FuyuanHuang HongbinQi ChunhuiTang YaoLi PeirongHe JianzhongZhao ZhijuLu GangXiao Fei - Distal metastasis remains a major clinical challenge in neuroblastoma (NB), the most common extracranial solid tumor in children. However, the molecular mechanisms mediating tumor-endothelial crosstalk and NB metastasis remain incompletely understood. By integrating single-cell omics analyses of clinical NB samples with experimental validations, we established the molecular subtypes of NB and identified a C2 subtype marked by MYCN amplification and dual positivity for TWIST1 and TAC1 expressions. This aggressive tumor subpopulation exhibited enhanced secretion of the neuropeptide substance P (encoded by TAC1), which was regulated by the transcription factor TWIST1. TAC1 signaled to tumor-associated endothelial cells with elevated TACR1 expression, consequently leading to endothelial senescence and disrupted vascular integrity. Remarkably, TAC1 overexpression was sufficient to accelerate NB tumorigenesis, circulating tumor cell (CTC) generation and metastatic progression in vivo. Clinically, TWIST1TAC CTCs were significantly enriched in the blood samples of metastatic NB patients compared to the non-metastatic group. As a proof-of-principle study, we further demonstrated that the TACR1 antagonist aprepitant could effectively suppress endothelial senescence, tumorigenesis, and CTC-mediated metastatic progression in vivo, presenting a potential therapeutic strategy for NB patients with TAC1-TACR1 activation. - Source: PubMed
Publication date: 2026/04/13
Liu XuefeiWang YutingCheng YixinYuan XiuliLi YiLian JingruDuan YifeiZheng ShuqianWu ChunHuang GuanyinZhao BoxiHu JianyangZhang BinyuXu HuanliLiu ChaoDuan LianhuiDong RuiHong XinWen Feiqiu - Pancreatic neuroendocrine tumors (PNETs) lack clinically validated biomarkers for risk stratification and treatment selection. p62 (also known as SQSTM1)-a multifunctional adaptor protein degraded by autophagy-has been associated with adverse outcomes, but its correlation with invasion and metastasis in PNETs remains unclear. We retrospectively analyzed 194 PNETs resected between January 1994 and December 2022. The expression of p62, LC3B, E-cadherin, and Twist1 was evaluated using immunohistochemistry, and targeted transcriptomic profiling (nCounter) was performed to compare p62-high and p62-low groups. High p62 expression was associated with shorter overall and disease-free survival and higher frequencies of lymph node metastasis and an infiltrating growth pattern. In tumors with an infiltrating growth pattern, p62 expression was higher at the invasive front than in the tumor center, supporting a spatial association with histopathologic invasion. Transcriptomic profiling showed enrichment of epithelial-mesenchymal transition (EMT) pathways in the p62-high group, including upregulation of TWIST1, a key EMT-related transcription factor. Consistently, p62-high tumors showed reduced membranous E-cadherin and increased cytoplasmic and nuclear Twist1 expression. In a subgroup of small tumors (≤ 20 mm), p62-high status was not associated with significantly different survival, but it remained associated with infiltrative histopathologic features. Collectively, high p62 expression was associated with an aggressive, infiltrative PNET phenotype and an EMT/Twist1-associated signature, suggesting that p62 may capture a biologic state characterized by infiltrative behavior and complement risk stratification within current WHO frameworks. - Source: PubMed
Publication date: 2026/04/10
Matsumoto TakashiYamamoto TakeoOsajima SatoruNakanishi YoshiyukiNoguchi ShokoMizuuchi YusukeMurakami MasatoshiUeda KeijiroTakigawa KenShimo MasatoshiMiyawaki KohtaKato KojiFujimori NaoNakata KoheiAishima ShinichiOda Yoshinao - Copyright: © 2026 Adeyika et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Aberrant DNA methylation changes lead to abnormal gene expression that contributes to the development and progression of prostate cancer (PCa). Inquiry of genome-wide DNA methylation dataset, we identified the homeodomain pancreatic and duodenal homeobox 1 (PDX1) gene as differentially hypermethylated in PCa compared to normal prostate tissues. Immunohistochemical analysis of matched PCa and normal prostate tissues using tissue microarray showed a significant 2.33-fold (p = 0.0001) higher PDX1 protein expression in the PCa compared to the normal prostate tissues. In PCa cell lines (PC-3 and LNCaP) engineered to stably overexpress or knockdown PDX1, the ectopic PDX1 expression significantly enhanced cell proliferation and migration, whereas PDX1 knockdown suppressed these phenotypic processes. Quantitative RT-PCR and Western blot analysis demonstrated that PDX1 overexpression was associated with increased expression of key metabolic regulators; INSR, IGF1R, CXCR4, CDH2, TWIST1, and SNAI1, whereas there is decreased expression of ESR2, and TNFα. Conversely, PDX1 knockdown led to the opposite effect in expression profiles of these metabolites. Notably, these effects were more pronounced under high-glucose conditions compared to low-glucose environments. Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways. Given its potential role in metabolic regulation, full insights into the function of PDX1 in PCa could contribute to improved treatment and prevention strategies, particularly for men with PCa and comorbidities such as obesity and diabetes. - Source: PubMed
Publication date: 2026/03/31
Adeyika Tayo ADatturgi AnjuEttinoffe YehnaraGhosh SomiranjanAlbanese ChristopherKwabi-Addo Bernard