ArticleJournal of Cancer2020
Loss of PDK4 expression promotes proliferation, tumorigenicity, motility and invasion of hepatocellular carcinoma cells.
Article in Journal of Cancer, 2020. 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, 24 citations in OpenAlex.
- Impact of aging on CD146Frontiers in bioengineering and biotechnology · 2026Article
- Beyond the convergence of metabolic reprogramming in primary liver cancer: a comprehensive review on energy and lipids metabolism.Frontiers in cell and developmental biology · 2026Review
- METTL14 modulates the nasopharyngeal carcinoma microenvironment via mFrontiers in immunology · 2026Article
- The efferocytosis-related genes of SLC26A6, TYRO3, and PDK4 have been identified as predictors of prognosis in hepatocellular carcinoma and are associated with the immune status.International journal of medical sciences · 2026Article
- METTL14 Regulates the Expression of Genes Related to Interferon, Interleukin and MHC Class I in Nasopharyngeal Carcinoma Cells.Cancer medicine · 2025Article
- PDK4 as a tumor suppressor in gastric cancer: implications for metabolic regulation, immune modulation, and prognostic potential.Discover oncology · 2025Article
- Multi-Omics Integration: Predicting Progression and Optimizing Clinical Treatment of Hepatocellular Carcinoma Through Malignant-Cell-Related Genes.International journal of molecular sciences · 2025Article
- Investigating the function and targeting of MET protein as an oncogene kinase in pancreatic ductal adenocarcinoma: A microarray data integration.BioImpacts : BI · 2025Review
- Ketogenic diet reshapes cancer metabolism through lysine β-hydroxybutyrylation.Nature metabolism · 2024Article
- Unveiling the PDK4-centered rituximab-resistant mechanism in DLBCL: the potential of the "Smart" exosome nanoparticle therapy.Molecular cancer · 2024Article
- Prognostic value of RNA methylation-related genes in gastric adenocarcinoma based on bioinformatics.PeerJ · 2024Article
- High glucose promotes benign prostatic hyperplasia by downregulating PDK4 expression.Scientific reports · 2023Article
- Article
- Pyruvate Dehydrogenase Kinase 4 Deficiency Increases Tumorigenesis in a Murine Model of Bladder Cancer.Cancers · 2023Article
- The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.International journal of molecular sciences · 2022Review
- Reversing tozasertib resistance in glioma through inhibition of pyruvate dehydrogenase kinases.Molecular oncology · 2022Article
- Novel Prognostic Signatures of Hepatocellular Carcinoma Based on Metabolic Pathway Phenotypes.Frontiers in oncology · 2022Article
- Article
- mAging · 2021Article
- Pyruvate dehydrogenase kinases (PDKs): an overview toward clinical applications.Bioscience reports · 2021Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the roles and underlying mechanisms of other PDK family members (i.e., PDK1, PDK2 and PDK3) in tumor progression have been extensively investigated and are well understood, the functions and underlying molecular mechanisms of pyruvate dehydrogenase kinase 4 (PDK4) in the tumorigenesis and progression of various cancers [including hepatocellular carcinoma (HCC)] remain largely unknown. In this study, we examined the expression profile of PDK4 in HCC clinical tissue specimens and the roles of PDK4 in the proliferation, tumorigenicity, motility and invasion of HCC cells. The immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR) results revealed that PDK4 was significantly downregulated in the cohort of HCC clinical specimens. Additionally, PDK4 protein was found in both the nucleus and cytoplasm of HCC cells based on an immunofluorescence (ICC) assay, and PDK4 protein was also found in the nucleus and cytoplasm of cancer cells contained in HCC clinical specimens based on IHC. The CCK-8 assay and cell colony formation assay demonstrated that stable depletion of endogenous PDK4 by lentivirus-mediated RNA interference (RNAi) markedly promoted the proliferation of HCC cell lines (i.e., BEL-7402 and BEL-7404 cells) in vitro, while PDK4 silencing significantly enhanced the tumorigenic ability of BEL-7404 cells in vivo. In addition to enhance proliferation and tumorigenesis induced by PDK4 silencing, additional studies demonstrated that knockdown of PDK4 led to increase migration and invasion of BEL-7402 and BEL-7404 cells in vitro. Taken together, these findings suggest that the loss of PDK4 expression contributes to HCC malignant progression.
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