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Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment
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Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment
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Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment
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Journal Article
Hypermethylated gene ANKDD1A is a candidate tumor suppressor that interacts with FIH1 and decreases HIF1α stability to inhibit cell autophagy in the glioblastoma multiforme hypoxia microenvironment
2019
Overview
Ectopic epigenetic mechanisms play important roles in facilitating tumorigenesis. Here, we first demonstrated that ANKDD1A is a functional tumor suppressor gene, especially in the hypoxia microenvironment. ANKDD1A directly interacts with FIH1 and inhibits the transcriptional activity of HIF1α by upregulating FIH1. In addition, ANKDD1A decreases the half-life of HIF1α by upregulating FIH1, decreases glucose uptake and lactate production, inhibits glioblastoma multiforme (GBM) autophagy, and induces apoptosis in GBM cells under hypoxia. Moreover, ANKDD1A is highly frequently methylated in GBM. The tumor-specific methylation of ANKDD1A indicates that it could be used as a potential epigenetic biomarker as well as a possible therapeutic target.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/109
/ 13/31
/ 14
/ 14/19
/ 38
/ 38/77
/ 42
/ 45
/ 82
/ 82/51
/ Chromosomes, Human, Pair 15 - genetics
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Hypoxia
/ Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors
/ Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
/ Intracellular Signaling Peptides and Proteins - physiology
/ Medicine
/ Mixed Function Oxygenases - genetics
/ Mixed Function Oxygenases - metabolism
/ Neoplasm Proteins - genetics
/ Neoplasm Proteins - metabolism
/ Oncology
/ Recombinant Proteins - metabolism
/ Repressor Proteins - genetics
/ Repressor Proteins - metabolism
