Open AccessMiR-let-7a inhibits cell proliferation, migration, and invasion by down-regulating PKM2 in gastric cancer
Author(s) -
Ran Tang,
Chao Yang,
Xiang Ma,
Younan Wang,
Dakui Luo,
Chih Chia Huang,
Zekuan Xu,
Ping Liu,
Yang Li
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.6821
Subject(s) - pkm2 , anaerobic glycolysis , microrna , medicine , carcinogenesis , cancer , cancer research , warburg effect , transplantation , cell growth , pyruvate kinase , liver cancer , cancer cell , glycolysis , oncology , biology , gene , metabolism , biochemistry
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.