## Abstract The loss of the Y chromosome is a frequent numerical chromosomal abnormality observed in human prostate cancer. In cancer, loss of specific genetic material frequently accompanies simultaneous inactivation of tumor suppressor genes. It is not known whether the Y chromosome harbors such
Partial suppression of tumorigenicity in a human lung cancer cell line transfected with Krev-1
✍ Scribed by Jorge Caamano; Marion Dirado; Toshihiko Lizasa; Shigeru Momiki; Elma Fernandes; Curt Ashendel; Makoto Noda; Andres J. P. Klein-Szanto
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 853 KB
- Volume
- 6
- Category
- Article
- ISSN
- 0899-1987
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
A human non‐small‐cell lung carcinoma cell line, Calu‐6 (from an anaplastic carcinoma), was transfected with the Ki‐ras‐related anti‐oncogene K__rev__‐1. Several transfectant lines were obtained that showed a reduced tumorigenicity in nude mice with respect to the parental and control transfected cell lines. This decrease was approximately 50% in tumor incidence at 4 wk after subcutaneous inoculation of the transfected cells. In addition, the volume of the Calu‐6 revertant‐derived tumors was three to 10 times smaller than that of the equivalent tumors produced by inoculation of the control cell line transfected with the neomycin‐resistance gene. K__rev__‐1‐transfected cells that exhibited reduced tumorigenicity expressed K__rev__‐1 mRNA and had variable numbers of copies of the K__rev__‐1 gene. Moreover, K__rev__‐1 ‐transfected cells exhibited a more differentiated squamous epithelial morphology than the parental and control cell lines did. Moderately elevated levels of protein kinase C activity were detected in some revertant clones. Such activity correlated with the level of expression of K__rev__‐1 mRNA in most cases. In summary, K__rev__‐1 induced important morphological and biological changes in transfected Calu‐6 cells that we interpreted as partial reversion of the malignant phenotype. © 1992 Wiley‐Liss, Inc.
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