Heterodimerization of Bcl-2 and Bcl-XL with Bax and Bad in Colorectal Cancer

Authors

  • Takashi Hattori From the Department of Gastroenterology, Fujigaoka Hospital, Showa University, Fujigaoka, Aoba-ku, Yokohama, Japan
  • Nobuhiko Ookawa From the Department of Gastroenterology, Fujigaoka Hospital, Showa University, Fujigaoka, Aoba-ku, Yokohama, Japan
  • Rikiya Fujita From the Department of Gastroenterology, Fujigaoka Hospital, Showa University, Fujigaoka, Aoba-ku, Yokohama, Japan
  • Kunihiko Fukuchi Department of Clinical Pathology, School of Medicine, Showa University, Hatanodai, Shinagawa-ku, Tokyo, Japan

DOI:

https://doi.org/10.1080/028418600750013410

Abstract

The rate of cell loss owing to apoptosis is mediated by competitive dimerization with selective pairs of cell death antagonists (Bcl-2, Bcl-XL) and agonists (Bax, Bad). The aim of this study was to investigate which Bcl-2 family dimers had a critical factor in colorectal cancer. We analyzed the expression of Bcl-2, Bcl-XL, Bax, and Bad in normal-appearinging mucosa and colorectal tumor tissues by Western blotting after immunoprecipitation. Compared with the ratio of Bax-Bcl-2/total Bax in normal mucosa, the ratio was significantly reduced in tumors (p=0.02). In this series, the low ratio of Bad-Bcl-2/total Bcl-2 was associated with advanced tumor stages (p=0.02). A reduced heterodimerization of Bax with Bcl-2 may contribute to the development of colorectal cancer. The heterodimerization of Bad with Bcl-2 may be repressed in advanced tumor tissues, and may contribute to tumor growth in colorectal cancer.

Downloads

Download data is not yet available.

Downloads

Published

2000-01-01

How to Cite

Hattori, T., Ookawa, N., Fujita, R., & Fukuchi, K. (2000). Heterodimerization of Bcl-2 and Bcl-XL with Bax and Bad in Colorectal Cancer. Acta Oncologica, 39(4), 495–500. https://doi.org/10.1080/028418600750013410