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MicroRNA-488 inhibits proliferation and glycolysis in human prostate cancer cells by regulating PFKFB3.


ABSTRACT: Prostate cancer (PCa) remains the second leading cause of cancer-related death among men in the United States, and its molecular mechanism remains to be elucidated. Recent studies have suggested that microRNAs may play an important role in cancer development and progression. By analyzing the Gene Expression Omnibus dataset, we found lower expression for miR-488 in PCa than in normal tissues. Moreover, CCK-8, EdU, glucose uptake, and lactate secrete assays revealed that overexpression of miR-488 in PCa cell lines PC3 and DU145 resulted in inhibition of proliferation and glycolysis. In contrast, downregulation of miR-488 expression promoted proliferation and glycolysis in PCa cells. Using a bioinformatic approach and dual-luciferase reporter assays, we identified 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, isoform3 (PFKFB3), as a direct target of miR-488. Inhibition of PFKFB3 also suppressed PCa cell glycolysis and proliferation. Our study suggests that miR-488 inhibits PCa cell proliferation and glycolysis by targeting PFKFB3, and thus, miR-488 may be a novel therapeutic candidate for PCa.

SUBMITTER: Wang J 

PROVIDER: S-EPMC6768114 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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MicroRNA-488 inhibits proliferation and glycolysis in human prostate cancer cells by regulating PFKFB3.

Wang Jun J   Li Xiaojuan X   Xiao Zhaoming Z   Wang Yu Y   Han Yuefu Y   Li Jun J   Zhu Weian W   Leng Qu Q   Wen Yuehui Y   Wen Xinqiao X  

FEBS open bio 20190822 10


Prostate cancer (PCa) remains the second leading cause of cancer-related death among men in the United States, and its molecular mechanism remains to be elucidated. Recent studies have suggested that microRNAs may play an important role in cancer development and progression. By analyzing the Gene Expression Omnibus dataset, we found lower expression for miR-488 in PCa than in normal tissues. Moreover, CCK-8, EdU, glucose uptake, and lactate secrete assays revealed that overexpression of miR-488  ...[more]

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