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Targeting insulin-like growth factor-binding protein-3 by microRNA-125b promotes tumor invasion and poor outcomes in non-small-cell lung cancer.

Abstract Insulin-like growth factor-binding protein-3 acts as a tumor suppressor that inhibits the PI3K/AKT signaling pathway due to blocking insulin growth factor-1 binding to its receptor. We hypothesized that insulin-like growth factor-binding protein-3 might be targeted by microRNA-125b and promote tumor invasion and poor outcome in non-small-cell lung cancer via activation of the PI3K/AKT signaling pathway. Real-time polymerase chain reaction and immunohistochemistry were performed to determine the level of microRNA-125b, insulin-like growth factor-binding protein-3 messenger RNA, and phosphorylated-AKT expression in 105 tumors from non-small-cell lung cancer patients. Low insulin-like growth factor-binding protein-3 messenger RNA levels and positive phosphorylated-AKT expression were more commonly found in patients with high microRNA-125b tumors than low microRNA-125b tumors. A poorer overall survival and relapse-free survival were observed in patients with high microRNA-125b tumors than low-microRNA-125b tumors in p53-mutated patients, but not in p53-wild-type patients. Mechanistically, microRNA-125b promotes invasion ability in p53-mutated cells via the PI3K/AKT activation by targeting of insulin-like growth factor-binding protein-3, but this effect was not observed in p53-wild-type cells. An increase in phosphorylated-AKT expression due to targeting of insulin-like growth factor-binding protein-3 by microRNA-125b was responsible for cell invasion in p53-mutated cells. In conclusion, the microRNA-125b level promotes invasive ability in p53-mutated cells via PI3K/AKT activation by targeting of insulin-like growth factor-binding protein-3, thereby resulting in p53-mutated non-small-cell lung cancer patients with poor outcomes.
PMID
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Authors

Mayor MeshTerms
Keywords

MicroRNA-125b

non-small-cell lung cancer

outcome

p53 mutation

tumor invasion

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28378642
OWN - NLM
STAT- MEDLINE
DA  - 20170405
DCOM- 20170410
LR  - 20170410
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 4
DP  - 2017 Apr
TI  - Targeting insulin-like growth factor-binding protein-3 by microRNA-125b promotes 
      tumor invasion and poor outcomes in non-small-cell lung cancer.
PG  - 1010428317694316
LID - 10.1177/1010428317694316 [doi]
AB  - Insulin-like growth factor-binding protein-3 acts as a tumor suppressor that
      inhibits the PI3K/AKT signaling pathway due to blocking insulin growth factor-1
      binding to its receptor. We hypothesized that insulin-like growth factor-binding 
      protein-3 might be targeted by microRNA-125b and promote tumor invasion and poor 
      outcome in non-small-cell lung cancer via activation of the PI3K/AKT signaling
      pathway. Real-time polymerase chain reaction and immunohistochemistry were
      performed to determine the level of microRNA-125b, insulin-like growth
      factor-binding protein-3 messenger RNA, and phosphorylated-AKT expression in 105 
      tumors from non-small-cell lung cancer patients. Low insulin-like growth
      factor-binding protein-3 messenger RNA levels and positive phosphorylated-AKT
      expression were more commonly found in patients with high microRNA-125b tumors
      than low microRNA-125b tumors. A poorer overall survival and relapse-free
      survival were observed in patients with high microRNA-125b tumors than
      low-microRNA-125b tumors in p53-mutated patients, but not in p53-wild-type
      patients. Mechanistically, microRNA-125b promotes invasion ability in p53-mutated
      cells via the PI3K/AKT activation by targeting of insulin-like growth
      factor-binding protein-3, but this effect was not observed in p53-wild-type
      cells. An increase in phosphorylated-AKT expression due to targeting of
      insulin-like growth factor-binding protein-3 by microRNA-125b was responsible for
      cell invasion in p53-mutated cells. In conclusion, the microRNA-125b level
      promotes invasive ability in p53-mutated cells via PI3K/AKT activation by
      targeting of insulin-like growth factor-binding protein-3, thereby resulting in
      p53-mutated non-small-cell lung cancer patients with poor outcomes.
FAU - Wang, Hsiu-Hua
AU  - Wang HH
AD  - 1 Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical
      University, Taipei, Taiwan.
FAU - Wang, Yao-Chen
AU  - Wang YC
AD  - 2 Department of Internal Medicine, Chung Shan Medical University Hospital,
      Taichung, Taiwan.
FAU - Wu, De-Wei
AU  - Wu DW
AD  - 1 Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical
      University, Taipei, Taiwan.
FAU - Hung, Chin-Sheng
AU  - Hung CS
AD  - 3 Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical
      University, Taipei, Taiwan.
AD  - 4 Department of Surgery, School of Medicine, College of Medicine, Taipei Medical 
      University Hospital, Taipei, Taiwan.
AD  - 5 Division of General Surgery, Department of Surgery, Taipei Medical University
      Hospital, Taipei, Taiwan.
AD  - 6 Cancer Research Center, Taipei Medical University Hospital, Taipei, Taiwan.
FAU - Chen, Chih-Yi
AU  - Chen CY
AD  - 7 Department of Surgery, Chung Shan Medical University Hospital, Taichung,
      Taiwan.
FAU - Lee, Huei
AU  - Lee H
AD  - 1 Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical
      University, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (IGFBP3 protein, human)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 3)
RN  - 0 (MIRN125 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Carcinoma, Non-Small-Cell Lung/*genetics/metabolism/mortality/pathology
MH  - Cell Line, Tumor
MH  - Disease-Free Survival
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, p53
MH  - Humans
MH  - Insulin-Like Growth Factor Binding Protein 3/*genetics/metabolism
MH  - Lung Neoplasms/*genetics/metabolism/mortality/pathology
MH  - MicroRNAs/*metabolism
MH  - Neoplasm Invasiveness
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction
MH  - Survival Analysis
OTO - NOTNLM
OT  - MicroRNA-125b
OT  - non-small-cell lung cancer
OT  - outcome
OT  - p53 mutation
OT  - tumor invasion
EDAT- 2017/04/06 06:00
MHDA- 2017/04/11 06:00
CRDT- 2017/04/06 06:00
AID - 10.1177/1010428317694316 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Apr;39(4):1010428317694316. doi: 10.1177/1010428317694316.

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