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Phosphoinositide‐dependent kinase 1–associated glycolysis is regulated by miR‐409‐3p in clear cell renal cell carcinoma

Clear cell renal cell carcinoma (ccRCC) is the most popular kidney cancer in adults. Metabolic shift toward aerobic glycolysis is a fundamental factor for ccRCC therapy. MicroRNAs (miRNAs) are thought to be important regulators in ccRCC development and progression. Phosphoinositide‐dependent kinase...

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Published in:Journal of cellular biochemistry 2019-01, Vol.120 (1), p.126-134
Main Authors: Wang, Yongjun, He, Yanfa, Bai, Hongzhong, Dang, Yi, Gao, Jiangyan, Lv, Pei
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creator Wang, Yongjun
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description Clear cell renal cell carcinoma (ccRCC) is the most popular kidney cancer in adults. Metabolic shift toward aerobic glycolysis is a fundamental factor for ccRCC therapy. MicroRNAs (miRNAs) are thought to be important regulators in ccRCC development and progression. Phosphoinositide‐dependent kinase 1 (PDK1) is required for metabolic activation; however, the role of PDK1‐induced glycolytic metabolism regulated by miRNAs is unclear in ccRCC. So, the purpose of the current study is to elucidate the underlying mechanism in ccRCC cell metabolism mediated by PDK1. Our results revealed that miR‐409‐3p inhibited glycolysis by regulating PDK1 expression in ccRCC cells. We also found that miR‐409‐3p was regulated by hypoxia. Our results indicated that PDK1 facilitated ccRCC cell glycolysis, regulated by miR‐409‐3p in hypoxia. MiR‐409‐3p is a target gene of phosphoinositide‐dependent kinase 1 in clear cell renal cell carcinoma (ccRCC) cells and tissues, which is downregulated by hypoxia/hypoxia‐inducible factor 1‐α. MiR‐409‐3p decreases ccRCC cell survival ability and glycolysis.
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Metabolic shift toward aerobic glycolysis is a fundamental factor for ccRCC therapy. MicroRNAs (miRNAs) are thought to be important regulators in ccRCC development and progression. Phosphoinositide‐dependent kinase 1 (PDK1) is required for metabolic activation; however, the role of PDK1‐induced glycolytic metabolism regulated by miRNAs is unclear in ccRCC. So, the purpose of the current study is to elucidate the underlying mechanism in ccRCC cell metabolism mediated by PDK1. Our results revealed that miR‐409‐3p inhibited glycolysis by regulating PDK1 expression in ccRCC cells. We also found that miR‐409‐3p was regulated by hypoxia. Our results indicated that PDK1 facilitated ccRCC cell glycolysis, regulated by miR‐409‐3p in hypoxia. MiR‐409‐3p is a target gene of phosphoinositide‐dependent kinase 1 in clear cell renal cell carcinoma (ccRCC) cells and tissues, which is downregulated by hypoxia/hypoxia‐inducible factor 1‐α. 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subjects 3-Phosphoinositide-Dependent Protein Kinases - genetics
3-Phosphoinositide-Dependent Protein Kinases - metabolism
Adults
Carcinoma, Renal Cell - metabolism
Carcinoma, Renal Cell - pathology
Carcinoma, Renal Cell - surgery
Cell Hypoxia
Cell Line, Tumor
Cell Proliferation
clear cell renal cell carcinoma
Clear cell-type renal cell carcinoma
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Glucose - metabolism
Glycolysis
Humans
Hypoxia
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Kidney cancer
Kidney Neoplasms - metabolism
Kidney Neoplasms - pathology
Kidney Neoplasms - surgery
Kidneys
Metabolic activation
Metabolic rate
Metabolism
MicroRNAs - chemistry
MicroRNAs - metabolism
miRNA
miR‐409‐3p
Molecular Mimicry - genetics
Oxygen Consumption
phosphoinositide‐dependent kinase 1
Regulators
Transfection
title Phosphoinositide‐dependent kinase 1–associated glycolysis is regulated by miR‐409‐3p in clear cell renal cell carcinoma
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