Positive correlation between the expression of X-chromosome RBM genes (RBMX, RBM3, RBM10) and the proapoptotic Bax gene in human breast cancer
✍ Scribed by Fernando Martínez-Arribas; David Agudo; Marina Pollán; Francisco Gómez-Esquer; Gema Díaz-Gil; Raul Lucas; José Schneider
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 122 KB
- Volume
- 97
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
In a recent report, it has been postulated that the ubiquitous RBM proteins might constitute a novel family of apoptosis modulators. We measured the expression of the X‐chromosome RBM genes (RBMX, RBM3, and RBM10) in 122 breast cancers by means of differential RT‐PCR. Using the same method, we also studied the expression of the apoptosis‐related genes Bcl‐2 and Bax. Markers of hormone dependence (estrogen and progesterone receptors), proliferation (Ki67 and DNA‐ploidy), angiogenesis (VEGF and CD105), as well as oncogene (c‐erb‐B2), and tumor suppressor gene (p53) expression were also analyzed. The expression of all X‐chromosome RBM genes was significantly associated with the expression of the proapoptotic Bax gene (RBMX, P = 0.039; RBM3, P < 0.001; RBM10 large variant, P < 0.001; RBM10 small variant, P < 0.001). Furthermore, the expression of both RBM10 variants was significantly associated with the expression of the VEGF gene (large variant, P = 0.004; small variant, P = 0.003). We also found an association of borderline significance (P = 0.05) between the expression of RBM3, the large variant of RBM10 and wild‐type p53. Expression of the small RBM10 variant, finally, was associated with high proliferation of the tumors (Ki67 ≥ 20%; P = 0.037). The expression of both RBM10 variants seems to be interdependent to a significant degree (r = 0.26, P = 0.006). From these results, it seems that the X‐chromosome, through its RBM genes, plays a formerly unknown role in the regulation of programmed cell death (apoptosis) in breast cancer. J. Cell. Biochem. 97: 1275–1282, 2006. © 2005 Wiley‐Liss, Inc.