Abstract 4000: Restoring LSAMP expression decreases the proliferation rate in osteosarcomas

Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL Osteosarcomas are the most common primary malignant tumors of bone. The tumors are highly aggressive with poor prognosis, and display complex genomic aberrations. Previously, our group has identified a frequently deleted region in 3q13.31 in osteosarcoma clinical samples and cell lines [1]. The deleted region contains non-coding RNA genes, pseudogenes and the gene encoding the limbic-system associated membrane protein (LSAMP). The latter has previously been reported to be a candidate tumor suppressor gene in other cancer types, and more recently in osteosarcomas. Interestingly, our data show that low expression of LSAMP is statistically correlated with shorter patient survival. To examine the possible function of LSAMP in osteosarcomas, the expression was restored in an osteosarcoma cell line with a homozygous deletion of the gene. Characterization of the cell line with restored LSAMP expression showed decreased proliferation rate, which is consistent with its suggested role as a tumor suppressor gene. The migration rate and colony forming capability of the cells were unaffected. Interestingly, gene expression profiling of the restored lines, showed up-regulation of three genes, all proposed to have a role in cancer biology. The results indicate that the LSAMP protein might up-regulate the transcription of these three genes, and that LSAMP alone, or in conjunction with other genes, suppresses tumors by reducing their proliferation rate. Together, our data strengthens the hypothesis of LSAMP being a tumor suppressor gene in osteosarcomas. 1. Kresse, S.H., et al., LSAMP, a Novel Candidate Tumor Suppressor Gene in Human Osteosarcomas, Identified by Array Comparative Genomic Hybridization. Genes Chromosomes & Cancer, 2009. 48(8): p. 679-693. 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 4000. doi:1538-7445.AM2012-4000