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Periostin promotes migration and invasion of renal cell carcinoma through the integrin/focal adhesion kinase/c-Jun N-terminal kinase pathway.

Abstract Periostin (POSTN) is an extracellular matrix protein which is overexpressed in a variety of cancers and has been related to tumorigenesis of renal cell carcinoma. However, the involvement of POSTN in renal cell carcinoma migration, invasion, and their underlying mechanisms has not been established. In this study, renal cell carcinoma cell lines stably overexpressing POSTN were established using a lentiviral vector, and the effects of POSTN on renal cell carcinoma cell migration and invasion were investigated. POSTN overexpression increased the migration and invasion capabilities of renal cell carcinoma cell lines as well as activity of matrix metalloproteinase-2 and matrix metalloproteinase-9. Integrin αvβ3 and αvβ5 antibodies inhibited POSTN overexpression or recombinant POSTN-induced focal adhesion kinase activation, cell migration, and invasion. Furthermore, lentivirus-mediated focal adhesion kinase knockdown and c-Jun N-terminal kinase inhibitor reduced POSTN-enhanced phosphorylation of c-Jun N-terminal kinase, matrix metalloproteinase-9 and matrix metalloproteinase-2 expressions, cell migration, and invasion. Our research thus indicates that POSTN promotes renal cell carcinoma cell migration and invasion through interaction with integrins αvβ3 and αvβ5 and subsequent activation of the focal adhesion kinase/c-Jun N-terminal kinase pathway. These results suggest that POSTN plays a critical role in renal cell carcinoma metastasis and may represent a potential target for novel therapeutic approaches against renal cell carcinoma.
PMID
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Authors

Mayor MeshTerms

Cell Movement

MAP Kinase Signaling System

Keywords

Periostin

cell invasion

cell migration

focal adhesion kinase/c-Jun N-terminal kinase pathway

integrin

renal cell carcinoma

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




PMID- 28381189
OWN - NLM
STAT- MEDLINE
DA  - 20170406
DCOM- 20170418
LR  - 20170418
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 4
DP  - 2017 Apr
TI  - Periostin promotes migration and invasion of renal cell carcinoma through the
      integrin/focal adhesion kinase/c-Jun N-terminal kinase pathway.
PG  - 1010428317694549
LID - 10.1177/1010428317694549 [doi]
AB  - Periostin (POSTN) is an extracellular matrix protein which is overexpressed in a 
      variety of cancers and has been related to tumorigenesis of renal cell carcinoma.
      However, the involvement of POSTN in renal cell carcinoma migration, invasion,
      and their underlying mechanisms has not been established. In this study, renal
      cell carcinoma cell lines stably overexpressing POSTN were established using a
      lentiviral vector, and the effects of POSTN on renal cell carcinoma cell
      migration and invasion were investigated. POSTN overexpression increased the
      migration and invasion capabilities of renal cell carcinoma cell lines as well as
      activity of matrix metalloproteinase-2 and matrix metalloproteinase-9. Integrin
      alphavbeta3 and alphavbeta5 antibodies inhibited POSTN overexpression or
      recombinant POSTN-induced focal adhesion kinase activation, cell migration, and
      invasion. Furthermore, lentivirus-mediated focal adhesion kinase knockdown and
      c-Jun N-terminal kinase inhibitor reduced POSTN-enhanced phosphorylation of c-Jun
      N-terminal kinase, matrix metalloproteinase-9 and matrix metalloproteinase-2
      expressions, cell migration, and invasion. Our research thus indicates that POSTN
      promotes renal cell carcinoma cell migration and invasion through interaction
      with integrins alphavbeta3 and alphavbeta5 and subsequent activation of the focal
      adhesion kinase/c-Jun N-terminal kinase pathway. These results suggest that POSTN
      plays a critical role in renal cell carcinoma metastasis and may represent a
      potential target for novel therapeutic approaches against renal cell carcinoma.
FAU - Chuanyu, Sun
AU  - Chuanyu S
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, China.
FAU - Yuqing, Zhu
AU  - Yuqing Z
AD  - 2 Department of Immunology, Shanghai Centre for Clinical Laboratory, Shanghai,
      China.
FAU - Chong, Xu
AU  - Chong X
AD  - 2 Department of Immunology, Shanghai Centre for Clinical Laboratory, Shanghai,
      China.
FAU - Guowei, Xia
AU  - Guowei X
AD  - 1 Department of Urology, Huashan Hospital, Fudan University, Shanghai, China.
FAU - Xiaojun, Zhao
AU  - Xiaojun Z
AD  - 2 Department of Immunology, Shanghai Centre for Clinical Laboratory, Shanghai,
      China.
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 (Cell Adhesion Molecules)
RN  - 0 (Integrin alpha5)
RN  - 0 (POSTN protein, human)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Carcinoma, Renal Cell/*pathology
MH  - Cell Adhesion Molecules/*physiology
MH  - Cell Line, Tumor
MH  - *Cell Movement
MH  - Focal Adhesion Protein-Tyrosine Kinases/*physiology
MH  - Humans
MH  - Integrin alpha5/physiology
MH  - JNK Mitogen-Activated Protein Kinases/*physiology
MH  - Kidney Neoplasms/*pathology
MH  - *MAP Kinase Signaling System
MH  - Neoplasm Invasiveness
OTO - NOTNLM
OT  - Periostin
OT  - cell invasion
OT  - cell migration
OT  - focal adhesion kinase/c-Jun N-terminal kinase pathway
OT  - integrin
OT  - renal cell carcinoma
EDAT- 2017/04/07 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/07 06:00
AID - 10.1177/1010428317694549 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Apr;39(4):1010428317694549. doi: 10.1177/1010428317694549.

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