Abstract 3355: Clock genes DEC1 and BMAL1 regulate the expression of stem cell marker genes Sox2 and c-Myc in cervical cancer

Abstract

Abstract It has been reported that abnormalities of clock genes are associated with tumor progression. Clock genes CLOCK, BMAL1/2, Differentiated embryonic chondrocyte gene (DEC)1/2, PER1/2/3 and CRY1/2 play important roles in the regulation of cell proliferation, cell cycle, apoptosis, epithelial to mesenchymal transition (EMT) and metastasis. We have shown that DEC1 is highly expressed in pancreatic cancer and oral cancer cells compared with non-tumor cells. However, the expression of clock genes is not well understood in cervical cancer. In this study, we focused on the expression of DEC1, DEC2 and BMAL1 in human cervical cancer tissues, examining their expression in biopsy and surgical resection samples by immunohistochemistry. As a result, DEC1 was strongly positive in tumor cells compared with adjacent non-tumor cells. Especially, the positive cells were observed in the front lesions of the tumors, suggesting that DEC1 is associated with invasion. The positive staining of vimentin was also observed in the same lesions where DEC1 was positive. On the other hand, no obvious significant difference in DEC2 expression was observed between tumor cells and non-tumor cells. For BMAL1, we found a week staining in the tumor cells compared with non-tumor cells. In addition, we examined the expression of stem cell marker Sox2 and c-Myc in cancer tissues. They were highly expressed in tumor cells compared with the adjacent non-tumor cells. Furthermore, Sox2 was expressed in metastatic lesions higher than the primary sites. These results suggest that clock genes DEC1 and BMAL1 may promote progression of cervical cancer, regulating Sox2 and c-Myc expression. Citation Format: Fuyuki Sato, Yasueru Muragaki. Clock genes DEC1 and BMAL1 regulate the expression of stem cell marker genes Sox2 and c-Myc in cervical cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3355.