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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Correlation of multidrug resistance with up-regulation of protein kinase C expression in KBV200 cells

Ya-wei Yuan1, Ai-min Sun, Chuan-gang Li

  • 1Department of Radiation Oncology1, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. yuanyawei@fangliao.com

Di 1 Jun Yi Da Xue Xue Bao = Academic Journal of the First Medical College of PLA
|November 25, 2005
PubMed
Abstract

Insights

Phorbol-12-myristate-13-acetate (PMA) activates protein kinase C (PKC) in KBV200 cells, significantly increasing their multidrug resistance (MDR). This suggests PKC plays a role in tumor cell MDR mechanisms.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Multidrug resistance (MDR) in cancer cells poses a significant challenge in chemotherapy.
  • Protein kinase C (PKC) is a family of enzymes implicated in various cellular processes, including drug resistance.

Purpose of the Study:

  • To investigate the expression of protein kinase C (PKC) in KBV200 cells.
  • To determine the association between PKC activity and multidrug resistance (MDR) in these cells.

Main Methods:

  • KBV200 cells were treated with phorbol-12-myristate-13-acetate (PMA), a PKC activator.
  • PKC activity was measured by assessing peptide substrate phosphorylation.
  • PKC isoform expression was analyzed using Western blotting.
  • Cell viability and inhibition rates were determined by MTT assay.

Main Results:

  • PMA treatment significantly increased total and membrane-bound PKC activity, while decreasing cytosolic PKC activity.
  • PKC-alpha expression was upregulated in the membrane fraction and downregulated in the cytosol.
  • PMA treatment increased the IC(50) values for vincristine and adriamycin, indicating enhanced drug resistance.
  • PKCbeta expression showed minor changes in the cytosol and no significant change in the membrane.

Conclusions:

  • PMA enhances the multidrug resistance of KBV200 cells.
  • These findings suggest a potential role for PKC in the mechanisms underlying tumor cell multidrug resistance.

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