MiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in gastric cancer
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Ran Tang1,*, Chao Yang2,*, Xiang Ma1,*, Younan Wang1, Dakui Luo1, Chi Huang1, Zekuan Xu1, Ping Liu3, Li Yang1
1Department of General Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
2Liver Transplantation Center of the First Affiliated Hospital and Key Laboratory on Living Donor Liver Transplantation, Ministry of Health, Nanjing Medical University, Nanjing, China
3Department of Oncology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
*These authors have contributed equally to this work
Li Yang, e-mail: email@example.com
Keywords: gastric cancer, microRNA-let-7a, PKM2
Received: June 08, 2015 Accepted: December 29, 2015 Published: January 05, 2016
In contrast to normal differentiated cells that depend on aerobicoxidation for energy production, cancer cells use aerobic glycolysis as the main source (Warburg’s effect). The M2 splice isoform of pyruvate kinase (PKM2) is the key regulator for the aerobic glycolysis, high expression of PKM2 contributes to the aerobic glycolysis, promotes the growth of tumors. In the present study, we found that PKM2 was highly expressed in gastric cancer (GC) tissues and had a strongly inverse correlation with the expression of microRNA-let-7a (miR-let-7a). Furthermore, we found that the overexpression of miR-let-7a markedly suppressed the proliferation, migration, and invasion of GC cells by down-regulating the expression of PKM2. MicroRNAs (miRNAs) are important regulators play key roles in tumorigenesis and tumor progression. Although previous reports showed that let-7 family members act as tumor suppressors in many cancers. The specific regulatory mechanism of miR-let-7a to PKM2 in gastric cancer is still unclear. In this study, we revealed that miR-let-7a function as the antitumor and gene regulatory effects of PKM2 in GC cells.
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