Abstract
Abstract P53 and RB protein is famous for its capacity to suppress tumor senescence pathway member. Senescence is a leading cause of cancer-related death, considerable uncertainty still remains about their effectiveness. However, each marker in an increased risk that experience genomic data with a cancer-specific mutations. So, senescence marker that techniques can't develop patient-specific treatment for particular about experimental study-conditions and result-analysis. This study was undertaken to evaluate the sm22 (smooth muscel protein 22-alpha) protein relation of senescence marker and changes condition of the radiation at human-link senescence marker genes. We were determined the expression of senescence-associated β-galactosidase and western-blot assay. It was performed in colon cancers that were 17 patients each of normal and adenoma, 16 patients each of normal and adenocarcinoma. To conformed enzyme efficiency is β-galactosidase, senescence pathway using of p16, p21 and p53. On the other hand, sm22 use of senescence marker in study. we have decided to micro-array analysis that 3 patients each of normal and adenoma, 2 patients each of normal and adenocarcinoma, 2 patients each of normal and irradiation-adenocarcinoma (2 weeks after) available miRNA sequences on the Agilent Human whole genome 8x60K array chip. Gene expression levels were calculated with Feature Extraction v10.7.3.1 (Agilent technologies, CA) Relative signal intensities for each gene were generated using the Robust Multi-Array Average algorithm. Senescence induced p16 expression in dependent β-galactosidase assay results, sm22 protein suppressed cellular senescence levels as well as p16 protein. The expression of p16 and sm22 was analyzed that not involved each normals, adenomas and adenocarcinomas tissue by western blot analysis. In addition, it found that these results were similar to those of micro array. The three groups (adenoma, adeno-carcinoma and irradiation-adeno-carcinoma) can be compared in terms of total 2-fold changed gene (least 200% of controls for up-regulated and lower than 50% of controls for down-regulated genes). We found this integrative data analysis tool to the LCN2, LYPD5 and LOC100132051 genes as well as CDKN2 (p16) and TAGLN2 (sm22) gene expression. Irradiation groups was much less than the adenoma (45.3 %) and adenocarcinoma (71.1 %) 2-fold changed gene expression. The LCN2, LYPD5 and LOC100132051 genes lower than adeno-carcinoma group level. Our observations suggest that shared gene and protein expression profiles may contribute to sm22 and p16 of senescence marker, irradiation induces cellular senescence of colon cancer. 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 3953. doi:1538-7445.AM2012-3953
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