ArticleApoptosis : an international journal on programmed cell death2026
Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Unveiling Lactylation: A Novel Frontier in Cancer Stemness and Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Histone lactylation: a novel epigenetic bridge linking cellular metabolism to benign and malignant gynecological diseases.Clinical epigenetics · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- Research progress on protein lactylation in female reproductive disease: molecular mechanisms, functions, and therapeutic implications.Frontiers in pharmacology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundEndometrial Cancer (EC) is one of the most prevalent malignancies in the female reproductive system. Hypoxia is a hallmark of the tumor microenvironment that drives metabolic reprogramming, endoplasmic reticulum (ER) stress, and aggressive behavior in cancer cells. However, the underlying mechanisms remain incompletely understood. This study aimed to investigate hypoxia-mediated regulation of EC progression, focusing on the role of SLC9A7 (Solute Carrier Family 9 Member A7, NHE7).
methodsEC cells were exposed to hypoxic conditions (1% O
resultsHypoxia promoted the malignant phenotypes and stemness of EC cells. NHE7 was identified as a potential target gene of the hypoxia pathway and was positively correlated with poor prognosis in EC. Furthermore, overexpression of NHE7 in xenografts accelerated tumor growth. Mechanistically, NHE7 enhanced oxidative phosphorylation (OXPHOS) by elevating COX6C (Cytochrome C Oxidase Subunit 6C) expression, further driving ER stress. Hypoxia-driven glycolysis elevated histone lactylation, which transcriptionally activated NHE7. This regulation was reversed by glycolysis or lactate production inhibitors.
conclusionHypoxia-driven glycolysis induces histone lactylation, leading to the upregulation of NHE7 expression. This process enhances OXPHOS-induced ER stress by upregulating COX6C expression, ultimately contributing to the malignant progression of EC.
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