Invade or proliferate? Two contrasting events in malignant behavior governed by p16(INK4a) and an intact Rb pathway illustrated by a model system of basal cell carcinoma

Cancer Res. 2003 Apr 15;63(8):1737-42.

Abstract

Using a highly infiltrative tumor type as basal cell carcinoma as the model system, we have examined the relation between invasive behavior and proliferation. Our results studying alterations in G(1)-S cell cycle regulatory proteins and proliferation in infiltrative cells were surprising and clearly indicated that invasion in tumors with an intact p16(INK4a)-cyclin D-retinoblastoma protein (Rb) pathway was equivalent to ceased proliferation. Using immunohistochemistry and Western blotting of microdissected parts of basal cell carcinomas, we showed that p16(INK4a) was up-regulated at the invasive front of the majority of basal cell carcinomas with infiltrative growth patterns, followed by ceased proliferation, as well as decreased phosphorylation of Rb. Besides supporting the fact that basal cell carcinomas have an intact Rb pathway, our results clearly indicate that invasive tumor cells change phenotype from a proliferative state to an invasive phenotype. Thus, invasion is not necessarily analogous with proliferation, implicating a paradigm shift in the understanding of two central processes in malignant behavior.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Carcinoma, Basal Cell / metabolism
  • Carcinoma, Basal Cell / pathology*
  • Cell Division / physiology
  • Cyclin D
  • Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p16 / physiology*
  • Cyclins / metabolism
  • Cyclins / physiology
  • Humans
  • Immunohistochemistry
  • Neoplasm Invasiveness
  • Retinoblastoma Protein / metabolism
  • Retinoblastoma Protein / physiology*
  • Skin Neoplasms / metabolism
  • Skin Neoplasms / pathology*
  • Up-Regulation

Substances

  • Cyclin D
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclins
  • Retinoblastoma Protein