HNF4
- Known as:
- HNF4
- Catalog number:
- E021043-2
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- EnoGene
- Gene target:
- HNF4
Related genes to: HNF4
- Gene:
- HNF4A NIH gene
- Name:
- hepatocyte nuclear factor 4 alpha
- Previous symbol:
- TCF14, MODY, MODY1
- Synonyms:
- NR2A1, HNF4
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-20
- Date modifiied:
- 2019-04-23
Related products to: HNF4
Related articles to: HNF4
- The Wnt/β-catenin and YAP pathways cooperatively drive gastrointestinal tumor progression. BCL2L1, a YAP target gene, encodes the anti-apoptotic isoform Bcl-xL, which is highly expressed in multiple cancers, but its role in gastric cancer remains unclear. - Source: PubMed
Publication date: 2026/09/08
Oya YukikoArai JunyaHayakawa YokuShiokawa ToshiroShinohara ShintaroHata MasahiroMatsushita YukiKinoshita HirotoUekura ChieKurokawa KenAbe SoheiTsuboi MayoIhara SozaburoSuzuki NobumiHikita HayatoTakehara TetsuroWang Timothy CFujishiro Mitsuhiro - The extracellular matrix (ECM) plays a central role in regulating tumor progression and metastatic colonization by providing biochemical and mechanical signals that shape cancer cell fate. However, most organoid culture systems rely on basement membrane extracts that fail to reproduce the tissue-specific extracellular environments encountered during metastasis. Here, we develop tissue-derived decellularized matrix hydrogels to reconstruct organ-specific microenvironments and investigate epigenetic adaptation to ECM cues during metastatic colonization. Patient-derived colorectal cancer organoids cultured in colon-derived matrices exhibited enhanced maintenance of stem-like phenotypes and colon-specific chromatin accessibility landscapes compared with cultures grown in basement membrane extracts, demonstrating improved physiological relevance for primary tumor modeling. When exposed to matrices derived from secondary organs, the organoids showed distinct growth phenotypes accompanied by rapid, tissue-dependent chromatin accessibility remodeling, indicating that ECM composition alone can reshape regulatory programs governing metastatic adaptation. Notably, liver-derived matrices selectively activated hepatocyte nuclear factor 4 alpha ()-associated transcriptional networks and created a context-specific dependence on c-MET signaling for survival. Functional perturbation of or c-MET signaling confirmed that both are required for organoid formation specifically within the liver matrix environment. Together, these findings establish tissue-derived matrix hydrogels as instructive bioactive materials that actively regulate cancer cell epigenetic states and reveal microenvironment-specific therapeutic vulnerabilities during early metastatic colonization. - Source: PubMed
Publication date: 2026/08/26
Yoon HeejeongKim DayoungJeong Hye-JinHan HohyeonKim Seon-JinJang JinahJung Deok-BeomMyung Seung-JaeYu Chang SikSong In HoChoi Ju HaeCorces M RyanKwon TaejoonMyung KyungjaeJoo JinmyoungKang Joo HPark Tae-EunCho Seung Woo - There is few research on which genes play an important role in tumors without lymph metastasis. This study aimed to identify candidate molecular alterations preferentially associated with N0-stage LUSC. - Source: PubMed
Publication date: 2026/08/31
Alipour MarzyehMoghanibashi MehdiNaeimi SirousMohamadynejad Parisa - Neuroendocrine carcinomas (NECs) comprise a highly heterogeneous group of lethal malignancies arising from diverse anatomical sites. - Source: PubMed
Publication date: 2026/08/26
Ge FanWang ZhanyuZheng SufeiWang GuibinLiu ChengmingWang XinfengLiu QingSun NanHe Jie - BHLHE40/DEC1 is a basic helix-loop-helix transcription factor (TF) that regulates circadian rhythm and T-cell responses. In hepatocytes, its function and interplay with other TFs are poorly understood. Employing a genome-wide approach, we show that its genomic binding strongly overlapped with that of carbohydrate response-element binding protein, a sugar-sensing TF and known inducer of BHLHE40 expression. Transcriptomic analysis of primary mouse hepatocytes revealed reduced expression of genes involved in genomic stability on Bhlhe40 knockdown by siRNA. Bhlhe40 depletion potentiated fructose responsiveness of genes involved in cell-cycle regulation. Strikingly, genomic binding of BHLHE40 extensively overlapped with enhancers occupied by PPARα, RXRα, and HNF4 nuclear receptors and BHLHE40 fine-tuned the expression of PPARα target genes. Using HEK293 cells, we further observed that BHLHE40 physically interacted with RXRα and PPARα cofactors. Collectively, our data suggest that through cooperation with carbohydrate response-element binding protein and nuclear receptors, BHLHE40 is a central regulator of hepatic gene expression with potential to integrate inputs from nutrient signals contributing to the metabolic flexibility of the liver. - Source: PubMed
Kokki KristaWowro Sylvia JRobciuc MariusHallasaari AttePorri LindaKinnunen MatiasStegmann Catrin APetricek Konstantin MVarjosalo MarkkuSchupp MichaelHietakangas Ville