PubTransformer

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PMID- 28373445
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - PI3K Catalytic Isoform Alteration Promotes the LIMK1-related Metastasis Through
      the PAK1 or ROCK1/2 Activation in Cigarette Smoke-exposed Ovarian Cancer Cells.
PG  - 1805-1818
AB  - AIM: To investigate the molecular mechanisms by which long-term exposure to
      cigarette smoke extract (CSE) contributes to ovarian cancer metastasis. MATERIALS
      AND METHODS: Western blot analysis for diverse p110 isoforms of phosphoinositide 
      3-kinase (PI3K)-related signaling pathway and epithelial-mesenchymal transition
      (EMT) markers was performed to analyze the underlying mechanisms. Migratory
      activity of CSE-exposed ovarian cancer cells was determined by transendothelial
      migration and invasion assay. RESULTS: After exposure to CSE for four weeks,
      CaOV3 (primary) and SKOV3 (metastatic) ovarian cancer cells showed enhanced
      mesenchymal characteristics and produced EMT-related cytokines [intwerleukin-8
      (IL-8), vascular endothelial growth factor (VEGF) and transforming growth
      factor-beta 1 (TGF-beta1)]. CSE exposure activated the Src-p110delta-p21
      protein-activated kinase 1 (PAK1) in CaOV3 cells and the
      Lyn-p110beta-Rho-associated kinases 1/2 (ROCK1/2) in SKOV3 cells, which led to
      the stimulation of LIM kinase 1 (LIMK1) phosphorylation and TGF-beta1 release.
      LIMK1 knockdown efficiently blocked the migratory activity and suppressed the
      mesenchymal phenotypes of CSE-treated ovarian cancer cells. Reactive oxygen
      species (ROS) initiated the CSE-mediated EMT processes in ovarian cancer cells.
      CONCLUSION: Characterization of the p110 isotypes of PI3K is critical for
      regulating cancer metastasis; LIMK1 could be a common therapeutic target of
      ovarian cancer metastasis.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Park, Ga Bin
AU  - Park GB
AD  - Department of Biochemistry, Kosin University College of Medicine, Busan, Republic
      of Korea.
FAU - Kim, Daejin
AU  - Kim D
AD  - Department of Anatomy, Inje University College of Medicine, Busan, Republic of
      Korea [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Cytokines)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (LIMK1 protein, human)
RN  - EC 2.7.11.1 (Lim Kinases)
RN  - EC 2.7.11.1 (PAK1 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (ROCK1 protein, human)
RN  - EC 2.7.11.1 (p21-Activated Kinases)
RN  - EC 2.7.11.1 (rho-Associated Kinases)
SB  - IM
MH  - Blotting, Western
MH  - Cell Movement/drug effects
MH  - Cell Proliferation/drug effects
MH  - Cytokines/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Epithelial-Mesenchymal Transition/drug effects
MH  - Female
MH  - Humans
MH  - Lim Kinases/antagonists & inhibitors/genetics/*metabolism
MH  - Neoplasm Metastasis
MH  - Ovarian Neoplasms/etiology/metabolism/pathology/*secondary
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Small Interfering/genetics
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
MH  - Smoking/*adverse effects
MH  - Transforming Growth Factor beta1/metabolism
MH  - Tumor Cells, Cultured
MH  - p21-Activated Kinases/*metabolism
MH  - rho-Associated Kinases/*metabolism
OTO - NOTNLM
OT  - *LIM kinase 1
OT  - *Phosphoinositide 3-kinase
OT  - *cigarette smoke extract
OT  - *epithelial-mesenchymal transition
OT  - *ovarian cancer
OT  - *p21 protein-activated kinase 1
OT  - *rho-associated kinases 1/2
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/01/31 [received]
PHST- 2017/03/05 [revised]
PHST- 2017/03/06 [accepted]
AID - 37/4/1805 [pii]
AID - 10.21873/anticanres.11515 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1805-1818.

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