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[Protein kinase D1 regulates the growth and metabolism of oral squamous carcinoma cells in tumor microenvironment].

AbstractOBJECTIVE:
To observe the effect of protein kinase D1 (PKD1) on the growth and metabolism of oral squamous cell carcinoma HSC-4 cells and related molecular mechanisms in the tumor microenvironment.
METHODS:
HSC-4 cell lines were transfected with shRNA plasmids. Three groups (Wild, control-shRNA, and PKD1-shRNA) were cultured under acidic or hypoxic environment for a certain time. Western blot was used to detect the expression of autophagy-related and glycolytic-related proteins. The proliferation changes were detected by CCK-8 kits.
RESULTS:
The PKD1-knockdown HSC-4 cell line was established. PKD1 silencing increased autophagy activity. Under hypoxic and acidic conditions, the PKD1-knockdown HSC-4 cells showed lower proliferation than the parental cells. PKD1-knockdown also decreased the expression of hypoxia induciblefactor 1α (HIF-1α) and pyruvate kinase M2 (PKM2).
CONCLUSIONS:
Under hypoxic and acidic conditions, PKD1 gene silencing can increase apoptotic autophagy activity. Downregulated PKD1 gene expression can reduce the glycolysis of oral squamous cell carcinoma cells and inhibit tumor cell proliferation. This study revealed the important role of PKD1 in the metabolism and growth of oral squamous cell carcinoma, making it a possible target for the treatment of oral squamous cell carcinoma.
AuthorsLi-Wei Wang, Yu Yu, Jiao Chen, Yun Feng, Bo-Miao Cui, Xiao-Ying Li, Jing-Nan Wang, Hong-Li Chen, Ping Zhang
JournalHua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology (Hua Xi Kou Qiang Yi Xue Za Zhi) Vol. 37 Issue 6 Pg. 577-582 (Dec 01 2019) ISSN: 2618-0456 [Electronic] China
PMID31875433 (Publication Type: Journal Article)
Chemical References
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Protein Kinases
Topics
  • Carcinoma, Squamous Cell
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Mouth Neoplasms
  • Protein Kinases
  • Tumor Microenvironment

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