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miR‐132 mediates a metabolic shift in prostate cancer cells by targeting Glut1

Prostate cancer is the second leading cause of cancer‐related deaths among men worldwide. Early diagnosis increases survival rates in patients but the survival rate has remained relatively poor over the past years. Increasing evidence shows that altered metabolism is a critical hallmark in prostate...

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Detalles Bibliográficos
Autores principales: Qu, Wei, Ding, Shi‐mei, Cao, Gang, Wang, She‐jiao, Zheng, Xiang‐hong, Li, Guo‐hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932453/
https://www.ncbi.nlm.nih.gov/pubmed/27398313
http://dx.doi.org/10.1002/2211-5463.12086
Descripción
Sumario:Prostate cancer is the second leading cause of cancer‐related deaths among men worldwide. Early diagnosis increases survival rates in patients but the survival rate has remained relatively poor over the past years. Increasing evidence shows that altered metabolism is a critical hallmark in prostate cancer. There is a strong need to explore the molecular mechanisms underlying cancer metabolism for prostate cancer therapy. Whether the aberrant expression of microRNA (miRNA) contributes to cancer metabolism is not fully known. In this study, we found that microRNA‐132 (miR‐132) expression is reduced and thus leads to a metabolic switch in prostate cancer cells. miR‐132 performs this role by increasing Glut1 expression, resulting in the enhanced rate of lactate production and glucose uptake. The altered metabolism induced by decreased miR‐132 levels confers the rapid growth of the cancer cells. These data indicate that miR‐132 is involved in regulating the Warburg effect in prostate cancer by inhibiting Glut1 expression.