ArticleCell communication and signaling : CCS2019
Estrogen inhibits autophagy and promotes growth of endometrial cancer by promoting glutamine metabolism.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 89 citations in OpenAlex.
- Unraveling the role of glutamine metabolism in cancer: from cell death mechanisms to tumor microenvironment modulation.Experimental hematology & oncology · 2026Review
- Amino Acids as Targets for Immunotherapy against Solid Tumors.Cell biochemistry and biophysics · 2026Review
- The role of estrogen and its receptors in the regulation of ferroptosis and autophagy.Molecular biology reports · 2026Review
- Multi-omics characterization of blood metabolites and cervical microbiota associated with estrus in simmental cattle.Animal microbiome · 2026Article
- Amino acids metabolism: a potential target for cancer treatment.Molecular cancer · 2025Review
- The Cold Atmospheric Plasma Inhibits Cancer Proliferation Through Reducing Glutathione Synthesis.Molecules (Basel, Switzerland) · 2025Article
- Estrogen Promotes Endometrial Cancer Development by Modulating ZNF626, SLK, and RFWD3 Gene Expression and Inducing Immune Inflammatory Changes.Biomedicines · 2025Article
- HLH-30/TFEB mediates sexual dimorphism in immunity inAutophagy · 2025Article
- Construction of cuproptosis-related genes risk model predicts the prognosis of Uterine Corpus Endometrial Carcinoma.Scientific reports · 2025Article
- Causal Relationships Between Pregnancy, Menstrual History, and Endometrial Cancer With Mediating Effects of Metabolism-Related Traits.Human mutation · 2025Article
- Cirsiliol suppresses malignant progression of hepatocellular carcinoma via regulation of glutamine metabolism.American journal of translational research · 2025Article
- Erianin inhibits endometrial cancer cell proliferation and migration by modulating glutamine metabolism through the ERK signaling pathway.American journal of translational research · 2025Article
- Metabolic Targets in CRC: The Emerging Role of Cytochrome P450 Inhibitors.Current pharmaceutical design · 2025Review
- Phosphocholine inhibits proliferation and reduces stemness of endometrial cancer cells by downregulating mTOR-c-Myc signaling.Cellular and molecular life sciences : CMLS · 2024Article
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- Association of glutaminase expression with immune-suppressive tumor microenvironment, clinicopathologic features, and clinical outcomes in endometrial cancer.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2024Article
- Progesterone inhibits endometrial cancer growth by inhibiting glutamine metabolism through ASCT2.Bioscience reports · 2024Article
- Advances in research on autophagy mechanisms in resistance to endometrial cancer treatment.Frontiers in oncology · 2024Review
- Tripartite motif containing 33 demonstrated anticancer effect by degrading c‑Myc: Limitation of glutamine metabolism and proliferation in endometrial carcinoma cells.International journal of oncology · 2023Article
- Identification and validation of a seven cuproptosis-associated lncRNA signature to predict the prognosis of endometrial cancer.The Journal of international medical research · 2023Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExcessive estrogen exposure is an important pathogenic factor in uterine endometrial cancer (UEC). Recent studies have reported the metabolic properties can influence the progression of UEC. However, the underlying mechanisms have not been fully elucidated.
methodsGlutaminase (GLS), MYC and autophagy levels were detected. The biological functions of estrogen-MYC-GLS in UEC cells (UECC) were investigated both in vivo and in vitro.
resultsOur study showed that estrogen remarkably increased GLS level through up-regulating c-Myc, and enhanced glutamine (Gln) metabolism in estrogen-sensitive UEC cell (UECC), whereas fulvestrant (an ER inhibitor antagonist) could reverse these effects. Estrogen remarkably promoted cell viability and inhibited autophagy of estrogen sensitive UECC. However, CB-839, a potent selective oral bioavailable inhibitor of both splice variants of GLS, negatively regulated Gln metabolism, and inhibited the effects of Gln and estrogen on UECC's growth and autophagy in vitro and / or in vivo.
conclusionsCB-839 triggers autophagy and restricts growth of UEC by suppressing ER/Gln metabolism, which provides new insights into the potential value of CB-839 in clinical treatment of estrogen-related UEC.
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