Effect of protein kinase C on multidrug resistance of multidrug-resistant colorectal cancer LoVo/Adr cells

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Qiang Ma1, Zhen-Shu Zhang, Ya-Li Zhang

  • 1Department of Gastroenterology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China. maqiang@fimmu.com

Di 1 Jun Yi Da Xue Xue Bao = Academic Journal of the First Medical College of PLA
|October 12, 2002
PubMed
Abstract

Insights

Protein kinase C (PKC) influences multidrug resistance in colorectal cancer cells. It affects adriamycin uptake through mechanisms independent of the mdr1 gene, highlighting novel therapeutic targets.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Multidrug resistance (MDR) is a significant challenge in colorectal cancer treatment.
  • Protein kinase C (PKC) is implicated in various cellular processes, including drug resistance.

Purpose of the Study:

  • To investigate the effect of PKC on the multidrug resistance of LoVo/Adr colorectal cancer cells.
  • To elucidate the underlying mechanisms of PKC-mediated drug resistance.

Main Methods:

  • PKC activity was measured using 32P incorporation following treatment with staurosporine (SP) and phorbol-12-myristate-13-acetate (PMA).
  • Adriamycin uptake was assessed by flow cytometry.
  • Reverse transcriptase-PCR was used to evaluate mdr1 gene expression.

Main Results:

  • PMA exhibited bidirectional regulation of PKC activity, while SP inhibited it.
  • Short-term PMA treatment decreased adriamycin uptake, whereas long-term treatment increased it.
  • Neither PMA nor SP altered the expression of the mdr1 gene.

Conclusions:

  • PKC plays a role in regulating multidrug resistance in colorectal cancer cells.
  • The mechanism involves pathways other than the direct regulation of mdr1 gene mRNA levels.

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