Abstract

Abstract Hepatocellular carcinoma is a common malignancy affecting approximately one million people worldwide annually. Recent studies have shown that appetite-associated nucleobindin-2 (NUCB-2) is over-expressed in clinical tumor samples such as gastric cancer, prostate cancer, renal cell carcinoma, endometrial carcinoma cells, colon cancer and breast cancer. The survival rate of high-level expression of NUCB-2 in cancer patients was lower than cancer patients with low-level expression of NUCB-2. In addition, overexpression of NUCB-2 was observed in liver cancer by using bioinformatics analysis. The liver cancer patients with NUCB-2 overexpression are associated with poor prognosis. However, the effect of NUCB-2 overexpression on tumor cells is still unclear. In this project, we evaluated the novel role and mechanisms of NUCB-2 overexpression in hepatoma cells. Our results indicated NUCB-2 mRNA expression level was induced by ER stress as determined with RT-PCR and real-time PCR, and induction of NUCB-2 protein level was significantly increased by ER stress. Increased ER stress by pre-S2Δ protein was significantly enhanced NUCB-2 expression. We also observed that the overexpression of NUCB-2 was corrected with ER stress in human hepatocellular carcinoma tumor samples. Consequently, this mechanistic research may provide a molecular basis to develop a biomarker and novel cancer chemotherapeutic agent for high level expression of NUCB-2 in cancer patients. keywords:Endoplasmic reticulum stress, Nucleobindin-2, real-time PCR, RT-PCR, HBV large surface mutant protein pre-S2Δ, Hepatocellular carcinoma, Huh-7, HepG2, MCF-7, Tunicamycin, Brefeldin A. Citation Format: Jui-Hsiang Hung, Hsiu-Ping Tsao, Ren-Hao Li, Chih-Han Li, Hut-Min Chang. To Investigate the mechanism and function of nucleobindin-2 in human hepatoma cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4884.

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