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Suppression of serum-induced c-jun expression by activated Ki-ras in human colon cancer cells

M Furuse1, S Shirasawa, K Okumura

  • 1Department of Genetics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-82, Japan.

The Japanese Journal of Human Genetics
|December 31, 2002
PubMed

Insights

Activated Ki-ras signaling in colon cancer cells suppresses c-jun gene induction via protein kinase C (PKC), not the c-Raf pathway. This finding clarifies how Ki-ras impacts immediate early gene expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Activated Kirsten rat sarcoma viral oncogene homolog (Ki-ras) is implicated in colon cancer development and gene expression deregulation.
  • Previous studies linked activated Ki-ras to altered c-myc expression in human colon cancer cell lines.

Purpose of the Study:

  • To investigate the relationship between Ki-ras-mediated signaling and the expression of immediate early genes, specifically c-jun.
  • To elucidate the regulatory mechanisms by which Ki-ras influences c-jun expression in colon cancer cells.

Main Methods:

  • Gene-targeting was used to create human colon cancer cell lines (HK2-6, HKe-3) with and without activated Ki-ras, derived from HCT116.
  • Analysis of c-jun expression upon serum stimulation.
  • Examination of protein kinase C (PKC) and c-Raf activity under serum-starved and stimulated conditions.

Main Results:

  • Serum-induced c-jun expression was rapid and strong in HKe-3 cells (with activated Ki-ras) but not in HCT116 or HK2-6 cells.
  • Phosphorylation of c-Raf was consistent across all cell lines.
  • Cytosolic PKC activity was approximately twofold higher in HKe-3 cells compared to HCT116 cells under both conditions.

Conclusions:

  • Activated Ki-ras appears to suppress the serum responsiveness of c-jun expression in colon cancer cells.
  • The suppression mechanism involves the protein kinase C (PKC) pathway, rather than the c-Raf pathway.

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