PLK1 as a potential prognostic marker of gastric cancer through MEK-ERK pathway on PDTX models

PLK1 has been identified as having a great effect on cell division and maintaining genomic stability in mitosis, spindle assembly, and DNA damage response by current studies. We assessed PLK1 expression in cervical cancer tissues and cells. We have also evaluated the effects of PLK1 on gastric cance...

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Bibliographic Details
Published in:OncoTargets and therapy 2018-01, Vol.11, p.6239-6247
Main Authors: Dang, Sheng-Chun, Fan, Yi-Yi, Cui, Lei, Chen, Ji-Xiang, Qu, Jian-Guo, Gu, Min
Format: Article
Language:English
Subjects:
Apoptosis
Breast cancer
Cancer therapies
Cell adhesion & migration
Cell cycle
Cell division
Cervical cancer
Chemotherapy
Deoxyribonucleic acid
Discovery tools
DNA
DNA damage
Evolution & development
Experiments
Gastric cancer
Gene amplification
Genomes
Kinases
Medical prognosis
Medical research
Metastasis
Original Research
Patients
Signal transduction
Studies
Surgery
Tumors
Xenografts
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Summary:PLK1 has been identified as having a great effect on cell division and maintaining genomic stability in mitosis, spindle assembly, and DNA damage response by current studies. We assessed PLK1 expression in cervical cancer tissues and cells. We have also evaluated the effects of PLK1 on gastric cancer cell proliferation, migration, and apoptosis both in vitro and in vivo. Our results show that PLK1 is overexpressed in gastric cancer tissues and cells. Inhibition of PLK1 contributes cell cycle G2-phase arrest and inhibits the proliferation, migration, and apoptosis of gastric cancer (GC) cells, whereas its overexpression promotes proliferation, migration, and apoptosis in these cells. Moreover, PLK1 inhibition reduces expression of pMEK and pERK. More importantly, in vivo by analyzing tumorigenesis in patient-derived tumor xenograft (PDTX) models, the inhibition of PLK1 activity by BI6727 significantly decreased the volume and weight of the tumors compared with control group (
ISSN:1178-6930
1178-6930
DOI:10.2147/OTT.S169880