HIF3A

Last update 08 May 2025

Basic Info

Synonyms

Basic-helix-loop-helix-PAS protein MOP7, bHLHe17, Class E basic helix-loop-helix protein 17

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Introduction

Acts as a transcriptional regulator in adaptive response to low oxygen tension. Acts as a regulator of hypoxia-inducible gene expression (PubMed:11573933, PubMed:16126907, PubMed:19694616, PubMed:20416395, PubMed:21069422). Functions as an inhibitor of angiogenesis in hypoxic cells of the cornea. Plays a role in the development of the cardiorespiratory system. May also be involved in apoptosis (By similarity). Attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes and hence inhibits HRE-driven transcriptional activation. Also inhibits hypoxia-inducible ARNT-mediated gene expression. Attenuates the ability of transcription factor HIF1A and EPAS1/HIF2A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes and hence inhibits HRE-driven transcriptional activation (PubMed:16126907, PubMed:17998805, PubMed:19694616, PubMed:20416395). May act as a tumor suppressor and inhibits malignant cell transformation (PubMed:17998805). Attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes and hence inhibits HRE-driven transcriptional activation. Attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes and hence inhibits HRE-driven transcriptional activation.

100 Clinical Results associated with HIF3A

100 Translational Medicine associated with HIF3A

0 Patents (Medical) associated with HIF3A

180

Literatures (Medical) associated with HIF3A

01 Feb 2025·IUBMB Life

Hypoxia inducible factor 3‐alpha promotes a malignant phenotype in colorectal cancer cells

Article

Author: Villanueva‐Herrero, Juan Antonio ; Fonseca Camarillo, Gabriela ; Castañeda Patlán, Maria Cristina ; Robles‐Flores, Martha ; Moreno‐Londoño, Angela Patricia ; Yamamoto‐Furusho, Jesús Kazuo ; Lopez‐Mejia, Alejandro ; de Leon‐Rendón, Jorge Luis

AbstractColorectal cancer (CRC) is the third most common cancer worldwide. Hypoxia is a hallmark of the tumor microenvironment, and cellular adaptation to it is primarily mediated by the family of Hypoxia‐inducible factors (HIFs) HIF‐1α, HIF‐2α, and HIF‐3α. However, in contrast to HIF‐1α and HIF‐2α, a specific role for HIF‐3α in cancer biology has not yet been clearly established. This research was aimed to elucidate the role of HIF‐3α in colon cancer. As reported previously for HIF‐1α and HIF‐2α, we found that HIF‐3α is also overexpressed under normoxic conditions in all cancer cell lines examined and in patient‐derived tumor tissue samples compared with non‐malignant cells and normal tissue, but remarkably, pulse‐chase experiments demonstrated that HIF‐3α displays high stability in cells compared with HIF‐1α and HIF‐2α. Progno Scan data analysis showed that overexpression of HIF‐3α correlated with a patient's lower survival rate and a poor prognosis in colon adenocarcinoma patients. Knockdown of HIF‐3α expression was carried out to investigate the effects derived from its silencing on malignant phenotype. We found a significative decrease in the Hypoxia Response Element (HRE) reporter transcriptional activity mediated by HIF‐3α and a reduction in cell viability under oxidative stress in colon cancer cells with HIF‐3α knockdown compared with control HIF‐3α expressing cells. In addition, HIF‐3α silencing also produced an increase in apoptotic rate, decreased clonogenic capacity, altered autophagy flux, and modulated the canonical Wnt/β pathway in an isoform‐dependent and cell context‐dependent manner in colon cancer cells. Overall, these data show that transcriptional activity mediated by HI3‐3α plays an essential role in promoting the malignant phenotype, cell survival, and resistance to cell death in CRC cells.

01 Feb 2025·iScience

Functional variant at 19q13.3 confers nonsyndromic cleft palate susceptibility by regulating HIF3A

Article

Author: Pan, Yongchu ; Du, Mulong ; Lou, Shu ; Ma, Lan ; Miao, Ziyue ; Li, Xiaofeng ; Li, Dandan ; Wang, Lin

This study investigates the genetic factors associated with nonsyndromic cleft palate only (NSCPO) through a two-stage genome-wide association study (GWAS) and functional experiments. A total of 311 NSCPO cases and 1,136 controls were included, and we identified rs3826795 in HIF3A significantly associated with NSCPO risk (p = 4.27E-09). Functional assays showed that the A allele of rs3826795 reduced VEZF1 binding to the HIF3A promoter, thereby enhancing HIF3A expression. Additionally, we demonstrated that HIF3A significantly influenced cellular processes, including apoptosis, proliferation, and migration, in both in vitro and in vivo models. Pathway enrichment analysis indicated that HIF3A suppressed the GABAergic synapse pathway, which plays a crucial role in embryonic development. These findings provide valuable insights into the genetic mechanisms underlying NSCPO susceptibility and suggest potential targets for future therapeutic interventions.

20 Jan 2025·Carcinogenesis

Epigenetic mechanisms underlying endometrial cancer outcomes: race-specific patterns of DNA methylation associated with molecular subtypes and survival

Article

Author: Keku, Temitope O ; Weissman, Bernard E ; Hoos, Emery ; Koval, Lauren E ; Olshan, Andrew F ; Corcoran, David L ; Bae-Jump, Victoria ; Rager, Julia E ; Nichols, Hazel B ; Fry, Rebecca C ; Roell, Kyle ; Tan, Xianming ; Godfrey, Sherette ; Eaves, Lauren A

AbstractEndometrial cancer (EC) is the fourth most common cancer in women in the USA. Stark racial disparities are present in EC outcomes in which Black women have significantly higher EC-related mortality than White women. The social and biologic factors that contribute to these disparities are complex and may include racial differences in epigenetic landscapes. To investigate race-specific epigenetic differences in EC tumor characteristics and outcomes, we utilized the most recent data within the Cancer Genome Atlas (TCGA). Genome-wide CpG methylation data for more than 850 000 CpG sites were analyzed across 245 tumor samples, including 52 from Black women and 181 from White women. Race-adjusted and race-stratified associations among CpG methylation in ECs and molecular subtypes and disease-free survival were examined. Race-specific analysis identified subtype-associated CpGs within 9572 genes in tumors from White women and only 10 genes in tumors that were from Black women. Race-specific analyses also identified survival-associated CpGs with 1119 unique genes identified in tumors from White women and none identified in tumors from Black women. Genes identified with differential methylation among subtypes included those involved in oxidative stress (HIF3A), and DNA repair (MLH1). Data from a replication cohort highlighted genes overlapping with those identified within the TCGA, such as G Protein Subunit Beta 1 (GNB1), involved in G-protein signaling, and Interleukin 37 (IL37), involved in cytokine signaling. Identification of these racial differences in EC tumor epigenetic landscapes and associated changes in gene expression may provide insight into strategies to improve outcomes and reduce disparities.

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HIF3A

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