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miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.

Abstract Tp53-induced glycolysis and apoptosis regulator (TIGAR) enhances the pentose phosphate pathway, thereby contributing directly to DNA repair due to generation of nicotinamide adenine dinucleotide phosphate (NADPH) and ribose-5-phosphate, two key precursors of DNA synthesis and repair. Targetscan database showed that miR-101 was predicted to potentially target TIGAR. Therefore, we speculated that miR-101 could enhance cisplatin-induced DNA damage by directly repressing TIGAR expression in prostate cancer cells. We found that upregulation of miR-101 inhibited viability, induced apoptosis, increased glycolysis rate and fructose-2,6-bisphosphate levels, decreased glucose-6-phosphate dehydrogenase expression and NADPH levels, and enhanced cisplatin-induced DNA damage in prostate cancer cells. We also demonstrated that TIGAR was a direct target of miR-101 by using luciferase activity assay. Furthermore, this study revealed that the roles of knockdown of TIGAR were similar to miR-101 upregulation in prostate cancer cells. Taken together, miR-101 inhibited viability, induced apoptosis, reprogramed glucose metabolism, and enhanced cisplatin-induced DNA damage through decreasing NADPH levels by directly suppressing the expression of TIGAR in prostate cancer cells.
PMID
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Authors

Mayor MeshTerms

Gene Expression Regulation, Neoplastic

Keywords

NADPH

TIGAR

glycolysis

miR-101

pentose phosphate pathway

prostate cancer

Journal Title dna and cell biology
Publication Year Start




PMID- 28384067
OWN - NLM
STAT- MEDLINE
DA  - 20170406
DCOM- 20170412
LR  - 20170412
IS  - 1557-7430 (Electronic)
IS  - 1044-5498 (Linking)
VI  - 36
IP  - 4
DP  - 2017 Apr
TI  - miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide
      Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced
      Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.
PG  - 303-310
LID - 10.1089/dna.2016.3612 [doi]
AB  - Tp53-induced glycolysis and apoptosis regulator (TIGAR) enhances the pentose
      phosphate pathway, thereby contributing directly to DNA repair due to generation 
      of nicotinamide adenine dinucleotide phosphate (NADPH) and ribose-5-phosphate,
      two key precursors of DNA synthesis and repair. Targetscan database showed that
      miR-101 was predicted to potentially target TIGAR. Therefore, we speculated that 
      miR-101 could enhance cisplatin-induced DNA damage by directly repressing TIGAR
      expression in prostate cancer cells. We found that upregulation of miR-101
      inhibited viability, induced apoptosis, increased glycolysis rate and
      fructose-2,6-bisphosphate levels, decreased glucose-6-phosphate dehydrogenase
      expression and NADPH levels, and enhanced cisplatin-induced DNA damage in
      prostate cancer cells. We also demonstrated that TIGAR was a direct target of
      miR-101 by using luciferase activity assay. Furthermore, this study revealed that
      the roles of knockdown of TIGAR were similar to miR-101 upregulation in prostate 
      cancer cells. Taken together, miR-101 inhibited viability, induced apoptosis,
      reprogramed glucose metabolism, and enhanced cisplatin-induced DNA damage through
      decreasing NADPH levels by directly suppressing the expression of TIGAR in
      prostate cancer cells.
FAU - Huang, Shiqiao
AU  - Huang S
AD  - 1 Department of Urology, Shandong Shanxian Central Hospital , Heze, People's
      Republic of China .
FAU - Yang, Zhiguo
AU  - Yang Z
AD  - 1 Department of Urology, Shandong Shanxian Central Hospital , Heze, People's
      Republic of China .
FAU - Ma, Yong
AU  - Ma Y
AD  - 1 Department of Urology, Shandong Shanxian Central Hospital , Heze, People's
      Republic of China .
FAU - Yang, Yiyong
AU  - Yang Y
AD  - 2 Department of Orthopedics, Shandong Shanxian Central Hospital , Heze, People's 
      Republic of China .
FAU - Wang, Shangren
AU  - Wang S
AD  - 1 Department of Urology, Shandong Shanxian Central Hospital , Heze, People's
      Republic of China .
LA  - eng
PT  - Journal Article
PL  - United States
TA  - DNA Cell Biol
JT  - DNA and cell biology
JID - 9004522
RN  - 0 (Antineoplastic Agents)
RN  - 0 (C12orf5 protein, human)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MIRN101 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 53-59-8 (NADP)
RN  - IY9XDZ35W2 (Glucose)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Antineoplastic Agents/toxicity
MH  - Apoptosis
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - Cisplatin/toxicity
MH  - DNA Damage
MH  - *Gene Expression Regulation, Neoplastic
MH  - Glucose/metabolism
MH  - Glycolysis
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/antagonists &
      inhibitors/*genetics/metabolism
MH  - Male
MH  - MicroRNAs/*metabolism
MH  - NADP/*metabolism
MH  - Prostatic Neoplasms/*genetics/metabolism/pathology
OTO - NOTNLM
OT  - NADPH
OT  - TIGAR
OT  - glycolysis
OT  - miR-101
OT  - pentose phosphate pathway
OT  - prostate cancer
EDAT- 2017/04/07 06:00
MHDA- 2017/04/13 06:00
CRDT- 2017/04/07 06:00
AID - 10.1089/dna.2016.3612 [doi]
PST - ppublish
SO  - DNA Cell Biol. 2017 Apr;36(4):303-310. doi: 10.1089/dna.2016.3612.

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