ArticleAmerican journal of cancer research2016
Inhibition of mTORC1 signaling sensitizes hepatocellular carcinoma cells to glycolytic stress.
Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Unraveling the pleiotropic roles of the mTOR-glycolytic axis in ulcerative colitis: from immunometabolic dysregulation to mucosal barrier remodeling.Frontiers in immunology · 2026Review
- The metformin administration on pancreatic tissue damage in metastatic rat prostate cancer and STZ induced diabetes model.Journal of molecular histology · 2025Article
- Multifaceted roles of lactate dehydrogenase in liver cancer (Review).International journal of oncology · 2025Review
- Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma.Current cancer drug targets · 2024Article
- PCBP1 regulates the transcription and alternative splicing of metastasis‑related genes and pathways in hepatocellular carcinoma.Scientific reports · 2021Article
- Prognostic value of eight immune gene signatures in pancreatic cancer patients.BMC medical genomics · 2021Article
- New insights into molecules and pathways of cancer metabolism and therapeutic implications.Cancer communications (London, England) · 2021Review
- The Role of RNA Methyltransferase METTL3 in Hepatocellular Carcinoma: Results and Perspectives.Frontiers in cell and developmental biology · 2021Review
- UBE2O promotes hepatocellular carcinoma cell proliferation and invasion by regulating the AMPKα2/mTOR pathway.International journal of medical sciences · 2021Article
- Metabolic reprograming of tumor-associated macrophages.Annals of translational medicine · 2020Review
- The combination of the glycolysis inhibitor 2-DG and sorafenib can be effective against sorafenib-tolerant persister cancer cells.OncoTargets and therapy · 2019Article
- Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease.Endocrine reviews · 2018Review
- The mTOR Pathway Regulates PKM2 to Affect Glycolysis in Esophageal Squamous Cell Carcinoma.Technology in cancer research & treatment · 2018Article
- Rapamycin (mTORC1 inhibitor) reduces the production of lactate and 2-hydroxyglutarate oncometabolites in IDH1 mutant fibrosarcoma cells.Journal of experimental & clinical cancer research : CR · 2017Article
- Impact of Metabolism on T-Cell Differentiation and Function and Cross Talk with Tumor Microenvironment.Frontiers in immunology · 2017Review
- Metabolic Hallmarks of Tumor and Immune Cells in the Tumor Microenvironment.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reprogrammed glucose metabolism, especially glycolysis, is profoundly implicated in tumor development or metastasis. As the interconnectedness and flexibility of metabolic signaling, targeting a metabolic signaling molecule may have limited anti-tumor effects. Here, Gene set enrichment analysis (GSEA) was used to explore the accompanied effectors of glycolysis in hepatocellular carcinoma (HCC). Based on the expression of lactate dehydrogenase A (LDHA), a key enzyme in catalyzing pyruvate into lactate, the glycolytic ability of HCC was defined as low group and high group. GSEA of two independent GEO datasets showed that mTORC1 signaling was the most striking metabolic alternations in high group. Pharmacological inhibition of mTORC1 signaling with rapamycin decreased LDHA level and glycolytic capacity of six HCC cell lines. Furthermore, c-Myc was identified as a downstream target of mTORC1 signaling and mediated mTORC1-induced LDHA expression. Importantly, rapamycin sensitized HCC cells to the glycolysis inhibitor 2-deoxyglucose (2-DG) in
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27822418PMC5088292W2562261475What OpenQuestion holds
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.