Increased actin cable organization after single chromosome introduction: Association with suppression of in vitro cell growth rather than tumorigenic suppression
✍ Scribed by Shingo Miyamoto; Makoto Nishida; Katsuhiro Miwa; Hidenori Kato; Toshiro Imamura; J. Carl Barrett; Motoyuki Shimizu; Mitsuo Oshimura; Norio Wake
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 1003 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0899-1987
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✦ Synopsis
Abstract
We previously showed that introduction of a single human chromosome 1, 6, or 9 derived from normal fibroblasts into HHUA endometrial carcinoma cells resulted in suppression of tumorigenicity. The tumorigenic suppression was accompanied by remarkable morphological changes in the microcell hybrids containing an extra copy of chromosome 1. The study presented here was undertaken to search for target cytoskeletal components affected by chromosome 1 transfer into endometrial carcinoma cells. We found that the microcell hybrids containing an extra copy of chromosome 1 were characterized by intracellular actin bundle formation and an excessive accumulation of actin and vinculin. The latter was a result of increased stabilization of the proteins. Additionally, chromosome 3 introduction into RCC23 human renal carcinoma cells resulted in prolongation of cell division and in senescence of a significant proportion of the microcell hybrids. In these microcell hybrids, the intracellular actin network was also reorganized, but the amounts of actin and vinculin protein were not increased. These findings suggest that the increased actin organization, which appeared not to cause tumorigenic suppression in the microcell hybrids, is associated with complementation of tumor suppressor genes and senescence by multiple mechanisms. © 1994 Wiley‐Liss, Inc.