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Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma.

Abstract Endometrial cancer is the most common gynecologic malignancy, about 80% of which is endometrial endometrioid carcinoma. Dysregulation of spindle assembly checkpoint plays a vital role in endometrial endometrioid carcinoma tumorigenesis and progression. The purpose of this study was to explore how tyrosine threonine kinase, a spindle assembly checkpoint-related protein, promotes the endometrial endometrioid carcinoma progression. We found that both messenger RNA and protein levels of tyrosine threonine kinase in endometrial endometrioid carcinoma tissues are higher than those in normal endometrial tissues, and its expression is associated with tumor stages. Genetic depletion of tyrosine threonine kinase by RNA interference in two endometrial endometrioid carcinoma cell lines significantly inhibits cell proliferation and induces apoptosis. Mechanistically, depletion of tyrosine threonine kinase induces G2/M cell cycle arrest and triggers caspase-dependent cell apoptosis. Collectively, tyrosine threonine kinase is significantly upregulated in endometrial endometrioid carcinoma, and downregulation of tyrosine threonine kinase can suppress endometrial endometrioid carcinoma cell proliferation and promote apoptosis via G2/M cell cycle arrest. Our study demonstrates that tyrosine threonine kinase can be a potential therapeutic target for endometrial endometrioid carcinoma treatment.
PMID
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Authors

Mayor MeshTerms
Keywords

Tyrosine threonine kinase

apoptosis

cell cycle arrest

endometrial endometrioid carcinoma

proliferation

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




PMID- 28718377
OWN - NLM
STAT- MEDLINE
DA  - 20170718
DCOM- 20170726
LR  - 20170726
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 7
DP  - 2017 Jul
TI  - Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest
      in human endometrioid endometrial adenocarcinoma.
PG  - 1010428317712444
LID - 10.1177/1010428317712444 [doi]
AB  - Endometrial cancer is the most common gynecologic malignancy, about 80% of which 
      is endometrial endometrioid carcinoma. Dysregulation of spindle assembly
      checkpoint plays a vital role in endometrial endometrioid carcinoma tumorigenesis
      and progression. The purpose of this study was to explore how tyrosine threonine 
      kinase, a spindle assembly checkpoint-related protein, promotes the endometrial
      endometrioid carcinoma progression. We found that both messenger RNA and protein 
      levels of tyrosine threonine kinase in endometrial endometrioid carcinoma tissues
      are higher than those in normal endometrial tissues, and its expression is
      associated with tumor stages. Genetic depletion of tyrosine threonine kinase by
      RNA interference in two endometrial endometrioid carcinoma cell lines
      significantly inhibits cell proliferation and induces apoptosis. Mechanistically,
      depletion of tyrosine threonine kinase induces G2/M cell cycle arrest and
      triggers caspase-dependent cell apoptosis. Collectively, tyrosine threonine
      kinase is significantly upregulated in endometrial endometrioid carcinoma, and
      downregulation of tyrosine threonine kinase can suppress endometrial endometrioid
      carcinoma cell proliferation and promote apoptosis via G2/M cell cycle arrest.
      Our study demonstrates that tyrosine threonine kinase can be a potential
      therapeutic target for endometrial endometrioid carcinoma treatment.
FAU - Zhang, Jiamiao
AU  - Zhang J
AD  - 1 Reproductive Medicine Center of the Affiliated Hospital, Guilin Medical
      University, Guilin, China.
FAU - Jiang, Yan
AU  - Jiang Y
AD  - 2 Department of Obstetrics and Gynecology of The Zhong Kang Hospital in
      Zhengzhou, Zhengzhou, China.
FAU - Zhao, Yu
AU  - Zhao Y
AD  - 3 Li Ka Shing Institute of Health Sciences and Prince of Wales Hospital, Chinese 
      University of Hong Kong, Hong Kong.
FAU - Wang, Wanxue
AU  - Wang W
AD  - 1 Reproductive Medicine Center of the Affiliated Hospital, Guilin Medical
      University, Guilin, China.
FAU - Xie, Yiran
AU  - Xie Y
AD  - 1 Reproductive Medicine Center of the Affiliated Hospital, Guilin Medical
      University, Guilin, China.
FAU - Wang, Huating
AU  - Wang H
AD  - 3 Li Ka Shing Institute of Health Sciences and Prince of Wales Hospital, Chinese 
      University of Hong Kong, Hong Kong.
FAU - Yang, Yihua
AU  - Yang Y
AD  - 1 Reproductive Medicine Center of the Affiliated Hospital, Guilin Medical
      University, Guilin, 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 (Protein Kinase Inhibitors)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
SB  - IM
MH  - Adenocarcinoma/*drug therapy/genetics/pathology
MH  - Apoptosis/drug effects
MH  - Carcinoma, Endometrioid/*drug therapy/genetics/pathology
MH  - Cell Cycle Checkpoints/drug effects
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects/genetics
MH  - Endometrial Neoplasms/*drug therapy/genetics/pathology
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - M Phase Cell Cycle Checkpoints/drug effects
MH  - Neoplasm Staging
MH  - Protein Kinase Inhibitors/*administration & dosage
MH  - Protein-Serine-Threonine Kinases/antagonists & inhibitors/genetics
MH  - Protein-Tyrosine Kinases/antagonists & inhibitors/genetics
MH  - RNA Interference
OTO - NOTNLM
OT  - Tyrosine threonine kinase
OT  - apoptosis
OT  - cell cycle arrest
OT  - endometrial endometrioid carcinoma
OT  - proliferation
EDAT- 2017/07/19 06:00
MHDA- 2017/07/27 06:00
CRDT- 2017/07/19 06:00
AID - 10.1177/1010428317712444 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jul;39(7):1010428317712444. doi: 10.1177/1010428317712444.