ArticleCellular & molecular biology letters2022
Metabolic disorders sensitise endometrial carcinoma through endoplasmic reticulum stress.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Endoplasmic reticulum stress in disease pathogenesis: its implications for therapy.Signal transduction and targeted therapy · 2026Review
- Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress.Apoptosis : an international journal on programmed cell death · 2026Article
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- Association of adherence to the EAT-Lancet diet and risk of uterine cancer: a prospective cohort from the UK Biobank.Frontiers in nutrition · 2026Article
- The Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in Gynecological Cancers: A Narrative Review.Cureus · 2025Review
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- Seneca Valley virus induces mitochondrial apoptosis by activating ER stress or the PERK pathway based on CaJournal of virology · 2025Article
- The role of reactive oxygen species in the pathogenesis and treatment of endometrial cancer.Frontiers in medicine · 2025Review
- Metabolism and epigenetics in cancer: toward personalized treatment.Frontiers in endocrinology · 2025Review
- Fer-mediated activation of the Ras-MAPK signaling pathway drives the proliferation, migration, and invasion of endometrial carcinoma cells.Molecular and cellular biochemistry · 2024Article
- Sesamolin serves as an MYH14 inhibitor to sensitize endometrial cancer to chemotherapy and endocrine therapy via suppressing MYH9/GSK3β/β-catenin signaling.Cellular & molecular biology letters · 2024Article
- Independent organelle and organelle-organelle interactions: essential mechanisms for malignant gynecological cancer cell survival.Frontiers in immunology · 2024Review
- Glutamine and amino acid metabolism as a prognostic signature and therapeutic target in endometrial cancer.Cancer medicine · 2023Article
- TMEM30A is essential for hair cell polarity maintenance in postnatal mouse cochlea.Cellular & molecular biology letters · 2023Article
- Genetics, environmental stress, and amino acid supplementation affect lactational performance via mTOR signaling pathway in bovine mammary epithelial cells.Frontiers in genetics · 2023Review
- Immunohistochemical Expression of IRE1 and PERK in Breast Cancer: Associations With Clinicopathological Characteristics and Survival Outcomes.Cancer diagnosis & prognosisArticle
- Unfolded protein response complexity in gynecological tumor dynamics: therapeutic challenges and future perspectives.Cell cycle (Georgetown, Tex.)Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMetabolic disorder is considered a well-established risk factor for endometrial carcinoma (EC). However, the mechanism remains unclear. Insulin resistance and excessive flux of free fatty acids serve as fundamental pathogenic factors in metabolic disorders, including obesity and type 2 diabetes. The aim of this study was to test the correlation between insulin resistance and dyslipidaemia in EC and to determine the effect of insulin and saturated fatty acids on EC cells.
methodsA retrospective study on the medical records of patients with EC and RNA-seq from the TCGA database analysed with edgR and Gene Ontology (GO) were used to assess the correlation of dyslipidaemia and diabetes as well as obesity. Crystal violet assays and CCK-8 assays were used to detect the proliferation of EC cells, and Annexin V-PI was used to examine apoptosis. Transient changes in mitochondrial Ca
resultsWe found that glucose metabolism disorders accompanied dyslipidaemia in patients with EC. As a key regulator of glucose metabolism disorders, insulin promoted DNA damage, ROS and Ca
conclusionsOur data are the first to illustrate that impaired glucose metabolism accelerates dyslipidaemia-promoted EC progression, which is attributed to hyperinsulinaemia and saturated fatty acid-induced Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.