Increased phosphorylation of nuclear phosphoproteins in human lung-cancer cells resistant to cis-diamminedichloroplatinum (II)

Int J Cancer. 1992 Feb 1;50(3):438-42. doi: 10.1002/ijc.2910500319.

Abstract

A novel non-phorbol-ester-like tumor promoter, okadaic acid (OA) has been shown to be an inhibitor of protein phosphatase I and IIA and, thus, to cause an "apparent activation" of protein kinase C (PKC). We previously showed that cis-diamminedichloroplatinum(II) (CDDP)-resistant cells, PC-9/CDDP, were cross-resistant to OA and that the cross-resistance was not due to the increased efflux of OA. We hypothesized that the phosphorylation status of some cellular proteins might be important in CDDP-resistance. No significant difference in PKC activity or total protein phosphatase activity measured in vitro was seen between PC-9 and PC-9/CDDP cells, nor in their sensitivity to inhibition by OA, nor in the amount of phosphorylation of whole cells or TCA-insoluble material. By SDS-PAGE after incubation of intact cells with 32P, we detected a marked increase, compared to PC-9 cells, in phosphorylation of the nuclear proteins of MW 32 and 20 kDa in CDDP-resistant PC-9/CDDP cells with no apparent difference in protein content. When phosphorylation of nuclear proteins observed in PC-9/CDDP cells was analyzed by 2-dimensional SDS-PAGE, the 32-kDa protein had a PI of about 4.5. The 32-kDa and 20-kDa bands were increased in a dose-dependent manner by CDDP treatment. On the other hand, no increase in phosphorylation of these proteins was observed in parental PC-9 cells. These results demonstrate a marked difference in the phosphorylation status of specific nuclear proteins between parental and CDDP-resistant cell lines, which may be related to CDDP-resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / drug therapy*
  • Adenocarcinoma / metabolism
  • Cell Nucleus / metabolism
  • Cisplatin / pharmacology*
  • Drug Resistance*
  • Electrophoresis, Gel, Two-Dimensional
  • Ethers, Cyclic / pharmacology
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Molecular Weight
  • Nuclear Proteins / metabolism*
  • Okadaic Acid
  • Phosphoprotein Phosphatases / metabolism
  • Phosphoproteins / metabolism*
  • Phosphorylation
  • Protein Kinase C / metabolism
  • Tetradecanoylphorbol Acetate / pharmacology
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Ethers, Cyclic
  • Nuclear Proteins
  • Phosphoproteins
  • Okadaic Acid
  • Protein Kinase C
  • Phosphoprotein Phosphatases
  • Tetradecanoylphorbol Acetate
  • Cisplatin