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[Correlation of protein kinase C isoform expression with multidrug resistance in KBV200 cells]

Ya-Wei Yuan1, Ai-Min Sun, Chuan-Gang Li

  • 1Department of Radiotherapy, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, China. ywyuan@163.net

Di 1 Jun Yi Da Xue Xue Bao = Academic Journal of the First Medical College of PLA
|October 23, 2002
PubMed
Abstract

Insights

Protein kinase C (PKC) may contribute to multidrug resistance (MDR) in KBV200 cells. Specifically, increased PKCalpha expression and activity appear to play a significant role in this MDR phenotype.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Pharmacology

Context:

  • Multidrug resistance (MDR) is a significant challenge in cancer chemotherapy.
  • KBV200 cells exhibit a multidrug-resistant phenotype.
  • Protein kinase C (PKC) signaling pathways are implicated in various cellular processes, including drug resistance.

Purpose:

  • To investigate the association between specific protein kinase C (PKC) isoforms and the multidrug resistance (MDR) mechanism in KBV200 cells.
  • To compare the expression and subcellular localization of PKC isoforms in drug-resistant KBV200 cells versus drug-sensitive parental KB cells.

Summary:

  • Western blotting and flow cytometry revealed higher PKC activity and an increased percentage of membrane-bound PKC in KBV200 cells.
  • PKCalpha expression was significantly elevated in KBV200 cells compared to parental KB cells, with unchanged PKCbeta and epsilon levels. PKCgamma and zeta were undetectable.
  • Increased fluorescence intensity of PKCalpha was observed in KBV200 cells, suggesting enhanced activity and membrane localization.

Impact:

  • These findings suggest that PKC signaling, particularly the PKCalpha isoform, may contribute to the development of the multidrug resistance (MDR) phenotype in KBV200 cells.
  • Understanding the role of PKCalpha in MDR could offer potential therapeutic targets for overcoming drug resistance in cancer treatment.

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