Abstract

Abstract Introduction: Deletion within the lung cancer tumour suppressor region at 3p21.3 constitutes the earliest premalignant chromosomal aberration in human lung cancers. Nineteen genes map to this region. RNA Binding Motif 5(RBM5) maps to one end of this 19-gene deletion breakpoint, and is not included in a slightly smaller 17-gene deletion that is common to breast and renal tumours. This suggests a critical role of RBM5 in lung cancers. To further explore the role of RBM5 in lung cancer, we examine the RBM5 expression in primary tissues and the associated function in vitro. Method: Paired non-tumor and tumor samples were obtained from 30 adenocarcinomas. The mRNA and protein expression of RBM5 were examined by semi-quantitative reverse transcription-polymerase chain reaction and Western blot. A549 cell line was used to determine the apoptotic function of RBM5 in vitro. A549 cells were transient transfected with RBM5, the AnnexinV, PAPP and cell cycle analysis were performed by flow cytometry and Western blot respectively. Results: We found that RBM5 mRNA and protein expression levels were reduced in tumor tissue compared the non-tumor tissue (P<0.05). Overexpression of RBM5 in A549 cells resulted in an increase of PAPP expression, phosphatidyl serine (PS) flip to the outer cellular membrane and G arrest in cell cycle. Conclusion: Decreased expression of RBM5 in adenocarcinomas suggests that RBM5 may play a crutial role in the carcinogenesis. Enhanced apoptotic activity induced by RBM5 overexpression in A549 cell line might be one of the essential mechanisms by which RBM5 function as a tumour suppressor. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3999. doi:1538-7445.AM2012-3999

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