Regulation of metabolic reprogramming by tumor suppressor genes in pancreatic cancer
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Experimental Hematology & Oncology Open Access
REVIEW
Regulation of metabolic reprogramming by tumor suppressor genes in pancreatic cancer Mengqi Liu1,2,3†, Wensheng Liu1,2,3†, Yi Qin1,2,3, Xiaowu Xu1,2,3, Xianjun Yu1,2,3*, Qifeng Zhuo1,2,3* and Shunrong Ji1,2,3
Abstract Background: Pancreatic cancer continues to be one of the most aggressive malignant tumors. Work in recent years in cancer molecular biology has revealed that metabolic reprogramming is an additional hallmark of cancer that is involved in the pathogenesis of cancers, and is intricately linked to gene mutations. Main text: However, though oncogenes such as KRAS and c-Myc play important roles in the process, and have been extensively studied, no substantial improvements in the prognosis of pancreatic cancer have seen. Therefore, some scientists have tried to explain the mechanisms of abnormal cancer metabolism from the perspective of tumor suppressor genes. In this paper, we reviewed researches about how metabolic reprogramming was regulated by tumor suppressor genes in pancreatic cancer and their clinical implications. Conclusion: Abnormal metabolism and genetic mutations are mutually causal and complementary in tumor initiation and development. A clear understanding of how metabolic reprogramming is regulated by the mutated genes would provide important insights into the pathogenesis and ultimately treatment of pancreatic cancer. Keywords: Tumor suppressor genes, Pancreatic cancer, Metabolic reprogramming, p53, Treatment Background Pancreatic cancer is one of the most aggressive forms of cancer and the fourth leading cause of cancer-related mortality both in men and women [1]. Although lots of money and efforts has been invested to study it, the results are disappointing. The overall 5-year survival rates of pancreatic cancer according to the latest data was only about 8%, even in the US where the best hospitals and cancer research institutions in the world are situated [1] An increasing body of research suggests that an additional hallmark of cancer is involved in the pathogenesis of cancer, that is, the capability to modify, or reprogram, *Correspondence: [email protected]; [email protected] † Mengqi Liu and Wensheng Liu contributed equally to this article 1 Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China 3 Pancreatic Cancer Institute, Fudan University, Shanghai Pancreatic Cancer Institute, Shanghai, China Full list of author information is available at the end of the article
cellular metabolism in order to support tumor proliferation [2]. For example, under aerobic conditions, normal cells process glucose, first to pyruvate via glycolysis in the cytoplasm and thereafter to oxidative phosphorylation in the mitochondria; while cancer cells consume glucose avidly but they only use a small amount for tricarboxylic acid (TCA) even in the presence of ample oxygen [3, 4]. This anomalous characteristic of cancer cell energy metabolism was first observed by Otto Warburg and is termed “ae
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