Expression and transformation ability of endogenous c-Maf transcription factor in gastric cancer cells

• Main Authors: I-Chen Chen, 陳奕辰
• Other Authors: Tien-Shun Yeh
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/18988547146483066015

碩士 === 國立陽明大學 === 解剖學及細胞生物學研究所 === 104 === According to the report of World Health Organization (WHO), gastric cancer is the fifth common cancer and the third mortality in the world. Patients with gastric cancer have a high re-currence rate and poor prognosis. In spite of various treatments, average overall survival of gastric cancer patient is less than one year. Although the incidence of gastric cancer is decreased, number of patients in East Asia is still on a rise. So far, the regulatory mechanism of gastric cancer stem cells (GCSCs) is still unclear. c-Maf transcription factor (v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog, proto-oncogene c-Maf) has been shown to play as an oncogene in multiple myeloma, and is involved in progressions of lymphoma and cholangiocarcinoma. However, its roles in gastric cancer carcinogenesis are still unknown. In this study, results showed that c-Maf expression levels of gastric cancer tissues were lower compared to normal stomach tissues. Knockdown of endogenous c-Maf expression promoted migration, invasion, colony formation, and tumor sphere formation ability in gastric cancer cells. Knockdown of endogenous c-Maf expression down-regulated expression levels of retinoblastoma protein (pRb), phospho-retinoblastoma protein (ppRb), cyclin B1, and p21. However, cyclin D1, γ-catenin of epithelial–mesenchymal transition (EMT) markers, and pluripotency marker proteins, including Nanog, Oct4 and SOX-2 were up-regulated. c-Maf also affected activity of pluripotency marker gene promoters. Moreover, overexpression of c-Maf decreased tumor growth in vivo. Suggesting that c-Maf plays a tumor-suppressive role in gastric cancer carcinogenesis.