ArticleCellular and molecular life sciences : CMLS2018
Crosstalk of protein kinase C ε with Smad2/3 promotes tumor cell proliferation in prostate cancer cells by enhancing aerobic glycolysis.
Article in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- An Evaluation of the Interaction of Brefeldin A with Mitogen-Activated Protein Kinase 1 (MAPK1) and Protein Kinase C Alpha (PrKCα): Insights from Molecular Modelling Studies.International journal of molecular sciences · 2026Article
- Cigarette Smoking-RegulatedEnvironment & health (Washington, D.C.) · 2026Article
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Article
- SMAD3 and HIF-1α orchestrate metabolic transition to aerobic glycolysis as a critical prerequisite for spontaneous reprogramming of spermatogonial stem cells.Stem cell research & therapy · 2025Article
- Zapotin mitigates breast cancer progression by targeting PKCε mediated glycolytic pathway regulation.BMC cancer · 2025Article
- Transcription factor ETS1‑mediated ECT2 expression promotes the malignant behavior of prostate cancer cells.Oncology letters · 2024Article
- A lactate-dependent shift of glycolysis mediates synaptic and cognitive processes in male mice.Nature communications · 2024Article
- Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis.Frontiers in pharmacology · 2024Article
- Article
- Elucidating the role of missense SNP of protein kinase C epsilon in HCV-induced hepatocellular carcinoma.BMC cancer · 2023Article
- Loss of Protein Kinase D2 Activity Protects Against Bleomycin-Induced Dermal Fibrosis in Mice.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Vitronectin Destroyed Intestinal Epithelial Cell Differentiation through Activation of PDE4-Mediated Ferroptosis in Inflammatory Bowel Disease.Mediators of inflammation · 2023Article
- Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells.Cell communication and signaling : CCS · 2022Article
- Targeting Protein Kinases and Epigenetic Control as Combinatorial Therapy Options for Advanced Prostate Cancer Treatment.Pharmaceutics · 2022Review
- Propofol suppresses cell proliferation in gastric cancer cells through NRF2-mediated polyol pathway.Clinical and experimental pharmacology & physiology · 2022Article
- The Interplay Between TGF-β Signaling and Cell Metabolism.Frontiers in cell and developmental biology · 2022Review
- Comprehensive analysis of aerobic glycolysis-related genes for prognosis, immune features and drug treatment strategy in prostate cancer.Frontiers in oncology · 2022Article
- miR-21-5p/PRKCE axis implicated in immune infiltration and poor prognosis of kidney renal clear cell carcinoma.Frontiers in genetics · 2022Article
- CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13.Journal of translational medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Protein kinase C ε (PKCε) has emerged as an oncogenic protein kinase and plays important roles in cancer cell survival, proliferation, and invasion. It is, however, still unknown whether PKCε affects cell proliferation via glucose metabolism in cancer cells. Here we report a novel function of PKCε that provides growth advantages for cancer cells by enhancing tumor cells glycolysis. We found that either PKCε or Smad2/3 promoted aerobic glycolysis, expression of the glycolytic genes encoding HIF-1α, HKII, PFKP and MCT4, and tumor cell proliferation, while overexpression of PKCε or Smad3 enhanced aerobic glycolysis and cell proliferation in a protein kinase D- or TGF-β-independent manner in PC-3M and DU145 prostate cancer cells. The effects of PKCε silencing were reversed by ectopic expression of Smad3. PKCε or Smad3 ectopic expression-induced increase in cell growth was antagonized by inhibition of lactate transportation. Furthermore, interaction of endogenous PKCε with Smad2/3 was primarily responsible for phosphorylation of Ser213 in the Samd3 linker region, and resulted in Smad3 binding to the promoter of the glycolytic genes, thereby promoting cell proliferation. Forced expression of mutant Smad3 (S213A) attenuated PKCε-stimulated protein overexpression of the glycolytic genes. Thus, our results demonstrate a novel PKCε function that promotes cell growth in prostate cancer cells by increasing aerobic glycolysis through crosstalk between PKCε and Smad2/3.
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