ArticleJournal of experimental & clinical cancer research : CR2018
STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- STK25 inhibits cancer-associated fibroblast activation to overcome cetuximab resistance in colorectal cancer.Clinical and translational medicine · 2026Article
- Identification of Novel Susceptibility Genes for Early-Onset Colorectal Cancer Through Germline Rare Variant Burden Testing.Cancers · 2025Article
- STK25 Loss Augments Anti-PD-1 Therapy Efficacy by Regulating PD-L1 Stability in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RBM5 suppresses proliferation, metastasis and glycolysis of colorectal cancer cellsWorld journal of gastrointestinal oncology · 2024Article
- The effects of metabolism on the immune microenvironment in colorectal cancer.Cell death discovery · 2024Review
- Prognostic value of oxidative stress-related genes in colorectal cancer and its correlation with tumor immunity.BMC genomics · 2024Article
- LncRNA-HOTAIRM1 promotes aerobic glycolysis and proliferation in osteosarcoma via the miR-664b-3p/Rheb/mTOR pathway.Cancer science · 2023Article
- NDR kinase tricornered genetically interacts with Ccm3 and metabolic enzymes in Drosophila melanogaster tracheal development.G3 (Bethesda, Md.) · 2023Article
- Role of glycolysis in inflammatory bowel disease and its associated colorectal cancer.Frontiers in endocrinology · 2023Review
- Glycolysis-related gene dihydrolipoamide acetyltransferase promotes poor prognosis in hepatocellular carcinoma through the Wnt/β-catenin and PI3K/Akt signaling pathways.Annals of translational medicine · 2022Article
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- STK25 enhances hepatocellular carcinoma progression through the STRN/AMPK/ACC1 pathway.Cancer cell international · 2022Article
- Exosomal miR-4800-3p Aggravates the Progression of Hepatocellular CarcinomaFrontiers in oncology · 2022Article
- Metformin prevents PFKFB3-related aerobic glycolysis from enhancing collagen synthesis in lung fibroblasts by regulating AMPK/mTOR pathway.Experimental and therapeutic medicine · 2021Article
- Vesicle transporter GOLT1B mediates the cell membrane localization of DVL2 and PD-L2 and promotes colorectal cancer metastasis.Cancer cell international · 2021Article
- Regulation of mTORC1 activity by the Golgi apparatus.Faculty reviews · 2021Review
- System Analysis of ROS-Related Genes in the Prognosis, Immune Infiltration, and Drug Sensitivity in Hepatocellular Carcinoma.Oxidative medicine and cellular longevity · 2021Article
- MiR-3150b-3p inhibits the progression of colorectal cancer cells via targeting GOLPH3.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2020Article
- p21International journal of molecular sciences · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSerine/threonine protein kinase 25 (STK25) is critical in regulating whole-body glucose and insulin homeostasis and the accumulation of ectopic lipids. The Warburg effect, also known as aerobic glycolysis, is an essential metabolic characteristic of cancer cells. However, the effects of STK25 on aerobic glycolysis of cancer cells remain unexplored. The aim of this study is to investigate the role of STK25 in colorectal cancer (CRC) and to elucidate the underlying mechanisms.
methodsThe influences of STK25 on the cell proliferation were evaluated by MTT and colony formation assays. The roles of STK25 in aerobic glycolysis were determined by glucose uptake and lactate production assays. The interaction between STK25 and GOLPH3 was detected by co-immunoprecipitation, GST pull-down, and His-tag pull-down assays. Western blot was used to measure the expression of glycolytic genes, and the status of kinases in mTOR pathway. Moreover, a xenograft mouse model was used to investigate the effects of STK25 in vivo. The prognostic significance of STK25 was analyzed using public CRC datasets by a log-rank test.
resultsSTK25 suppressed proliferation, glycolysis and glycolytic gene expression in CRC cells. STK25 interacted with GOLPH3 and mediated glycolysis through GOLPH3-regulated mTOR signaling. Consistent with these observations, silencing of STK25 promoted tumor growth and glycolytic gene expression in an in vivo xenograft mouse model. Moreover, high levels of STK25 correlated with favorable prognosis in patients with CRC.
conclusionsOur results demonstrated that STK25 negatively regulates the proliferation and glycolysis via GOLPH3-dependent mTOR signaling. Accordingly, STK25 could be a potential therapeutic target for the treatment of CRC.
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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.