Abstract 1139: Ras association domain family protein 1, isoform C (RASSF1C) promotes breast tumor growthin vivo

Mark E. Reeves, Robert J. Aragon, Mariana Alfakouri, Shin-Tai Chen, Yousef G. Amaar

Research output: Contribution to journalMeeting abstractpeer-review

Abstract

Breast cancer will kill more than 40,000 women in the United States this year, second in cancer deaths only to carcinoma of the lung. Therefore, a better understanding of the molecules and pathways that lead to breast cancer development is important because it could lead to specific therapies that interrupt these pathways. Recently, the Ras association domain family 1 (RASSF1) gene was identified as a Ras effector that plays an important role in carcinogenesis. The RASSF1 gene encodes two major isoforms, RASSF1A and RASSF1C, derived by alternative promoter selection and alternative mRNA splicing. While RASSF1A is extensively studied and is an established tumor suppressor, very little is known about RASSF1C functionOur laboratory is interested in determining the role of RASSF1C in human cancer cell growth. We have previously shown that of RASSF1C promotes cell proliferation and migration and attenuates apoptosis of breast cancer cells in vitro. To confirm our hypothesis that RASSF1C may be a growth promoter, we have tested the growth of human breast cancer cells over-expressing RASSF1C in nude mice. Our preliminary studies show that breast cancer cells over-expressing RASSF1C developed significantly larger tumors compared to control cells. We have confirmed the expression of RASSF1C in tumor tissue using both RT-PCR and immune-staining analyses. Together, our previous in vitro and current in vivo findings further support our hypothesis that RASSF1C, unlike RASSF1A, is not a tumor suppressor and rather it appears to play a role in stimulating proliferation and survival of breast cancer cells.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1139. doi:10.1158/1538-7445.AM2011-1139
Original languageAmerican English
Pages (from-to)1139-1139
Number of pages1
JournalCancer Research
Volume71
Issue number8_Supplement
DOIs
StatePublished - Apr 15 2011

Disciplines

  • Oncology
  • Medicine and Health Sciences
  • Bioinformatics

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