Abstract
BackgroundRibosomal proteins are the components of ribosome, which also exhibit various secondary functions in DNA repair, apoptosis, drug resistance and proliferation. In our previous study of microarray, ribosomal protein L15 (RPL15) was identified as an upregulated gene in gastric cancer.MethodsWe investigated the expression of ribosomal protein L15 in gastric cancer and the effect of RPL15 on proliferation of gastric cancer.ResultsIt was found that the expression of RPL15 was markedly up-regulated in gastric cancer tissues. RPL15 was also highly expressed in gastric cancer cell lines AGS, MKN45, MKN28, SGC7901 and KATOIII. Inhibition of RPL15 expression by siRNA vector transfection suppressed the growth of SGC7901 cells significantly, which was independent of the expression of Cyclin D1 and B1. Down-regulation of RPL15 expression inhibited SGC7901 cell growth in soft agar and its tumorigenicity in nude mice.ConclusionRPL15 promotes cell proliferation and may be a potential target for anticancer therapy of gastric cancer.
Highlights
Ribosomal proteins are the components of ribosome, which exhibit various secondary functions in DNA repair, apoptosis, drug resistance and proliferation
Expression of ribosomal protein L15 (RPL15) in gastric cancer tissues and cell lines To examine whether the RPL15 expression level is altered in gastric cancer, the expression and subcellular localization of RPL15 were studied in a set of gastric cancer patient specimens derived from 23 normal gastric mucosae (NG), 23 gastric cancer (GC) and 23 adjacent nontumorous tissues (NT)
The RPL15 staining in gastric cancer cells was consistently stronger than those of the NG
Summary
Ribosomal proteins are the components of ribosome, which exhibit various secondary functions in DNA repair, apoptosis, drug resistance and proliferation. Loss of heterozygosity (LOH) on loci of chromosomes 1, 5, 7, 12, 13 and 17 were frequently identified in advanced gastric carcinomas [3] Genetic alterations such as activation of oncogenes and inactivation of tumor suppressor genes could often be found in gastric cancer. It was believed that mutation or amplification of oncogenes c-ras, c-erbB-2, K-sam, c-met, and c-myc and inactivation of tumor suppressor genes p53, adenomatosis polyposis coli (APC), deleted in colorectal carcinomas (DCC), and retinoblastoma (RBI) are related to the development of gastric cancer. These genes (page number not for citation purposes)
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