[Silencing of PKG1 expression enhances the efficacy of vemurafenib against melanoma cell]

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2017 Apr 8;33(4):289-293. doi: 10.12047/j.cjap.5559.2017.071.
[Article in Chinese]

Abstract

Objective: To explore whether targeting phosphoglycerate kinase 1 (PGK1) can enhance the sensitivity of BRAFV600E mutation melanoma cells to vemurafenib.

Methods: The methods of cell biology, molecular biology and pharmacology(MTT assay, Western blot, FCM, Colongenic assay) were used in this study.

Results: ① Silencing of PGK1 expression increased the efficacy of vemurafenib in melanoma cells, as evidenced by greater killing in the tumor cells subjected to combined treatment of vemurafenib with siPGK1; ②The mechanism of enhanced sensitivity of melanoma cells to vemurafenib was associated with activation of apoptotic signaling pathway.

Conclusions: Targeting of PGK1 may represent a novel strategy of sensitizing melanoma cells to vemurafinib.

Keywords: PGK1; apoptosis; melanoma; vemurafenib.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Gene Silencing*
  • Humans
  • Indoles / pharmacology*
  • Melanoma / genetics*
  • Melanoma / pathology
  • Mutation
  • Phosphoglycerate Kinase / genetics*
  • Proto-Oncogene Proteins B-raf
  • Sulfonamides / pharmacology*
  • Vemurafenib

Substances

  • Antineoplastic Agents
  • Indoles
  • Sulfonamides
  • Vemurafenib
  • Proto-Oncogene Proteins B-raf
  • PGK1 protein, human
  • Phosphoglycerate Kinase