Conflict of Interest: None declared
Background: Activation

Conflict of Interest: None declared.
Background: Activation of the ubiquitin-proteasome pathway in various malignancies, including FTY720 clinical trial colorectal cancer, is established. This pathway mediates the degradation of damaged

proteins and regulates growth and stress response. The novel human gene, UBE2Q2, with a putative ubiquitin-conjugating enzyme activity, is reported to be overexpressed in some malignancies. We sought to investigate the expression levels of the UBE2Q2 gene in colorectal cell lines as well as in cancerous and normal tissues from patients with colorectal cancer. Inhibitors,research,lifescience,medical Methods: Levels of UBE2Q2 mRNA in cell lines were assessed by Real-Time PCR. Western blotting was employed to investigate Inhibitors,research,lifescience,medical the levels of the UBE2Q2 protein in 8 colorectal cell lines and 43 colorectal tumor samples. Results: Expression of UBE2Q2 was observed at the level of both mRNA and protein in colorectal cell lines, HT29/219, LS180, SW742, Caco2, HTC116, SW48, SW480, and SW1116. Increased levels of UBE2Q2 immunoreactivity was observed in the 65.11% (28 out of 43) of the colorectal carcinoma tissues when compared with their corresponding normal tissues. Difference between the mean intensities of UBE2Q2 bands from cancerous and normal tissues was statistically significant at P<0.001 (paired t test). Conclusion: We showed the expression pattern of the novel human gene, UBE2Q2, in 8 colorectal Inhibitors,research,lifescience,medical cell lines. Overexpression

of UBE2Q2 in the majority of the colorectal carcinoma samples denotes that it may have implications for the pathogenesis of colorectal cancer. Keywords: UBE2Q2, Colorectal Cancer, Inhibitors,research,lifescience,medical Cell Line, Gene Expression Introduction Colorectal cancer (CRC) is the third most common type of non-skin cancer worldwide and the third Inhibitors,research,lifescience,medical cause of cancer-related death in the Western world.1,2 The molecular defects in CRC can be due to changes that result in increased activity of oncogenes or to changes that lead to loss of function of the tumor-suppressor genes.3 A large

number of colorectal tumors show mutations in the KRAS oncogene as well as in the APC, p53, and SMAD4/DPC4 tumor-suppressor genes. An increasing number of mutated genes have been identified in CRC.3,4 These genes encode proteins with essential roles in CRC carcinogenesis.4 These proteins are shown to be regulated by the ubiquitin-proteasome system (UPS). This system regulates various cellular Parvulin processes by targeting proteins for activation, degradation, or localization at specific intracellular sites.4,5 Ubiquitin-mediated degradation of proteins is comprised of steps mediated by ubiquitin-activating enzymes (E1s), ubiquitin-conjugating enzymes (E2s), and ubiquitin ligases (E3s). The E1 enzyme activates ubiquitin and then transfers it to E2s. Subsequent conjugation of ubiquitin with the specific protein substrate is catalyzed by E2s alone or by E2s together with E3s.

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