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Tytuł:
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KIF18B as a regulator in microtubule movement accelerates tumor progression and triggers poor outcome in lung adenocarcinoma.
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Autorzy:
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Ji Z; Department of Respiratory Medicine, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu, 215028, PR China.
Pan X; Department of Nursing, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu, 215028, PR China.
Shang Y; Department of Respiratory and Critical Care Medicine, Changhai Hospital, Second Military Medical University, Shanghai, 200433, PR China.
Ni DT; Department of Respiratory Medicine, Suzhou Kowloon Hospital, Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu, 215028, PR China. Electronic address: .
Wu FL; Department of Oncology, First People Hospital of Lianyungang, Lianyungang, Jiangsu, 222002, PR China. Electronic address: .
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Źródło:
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Tissue & cell [Tissue Cell] 2019 Dec; Vol. 61, pp. 44-50. Date of Electronic Publication: 2019 Sep 03.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: Edinburgh : Churchill Livingstone
Original Publication: Edinburgh, Oliver & Boyd.
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MeSH Terms:
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Disease Progression*
Movement*
Adenocarcinoma of Lung/*metabolism
Adenocarcinoma of Lung/*pathology
Kinesins/*metabolism
Lung Neoplasms/*metabolism
Lung Neoplasms/*pathology
Microtubules/*metabolism
A549 Cells ; Adenocarcinoma of Lung/genetics ; Cell Movement/genetics ; Cell Proliferation/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/genetics ; Male ; Middle Aged ; Neoplasm Invasiveness ; Prognosis ; Proportional Hazards Models ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; Treatment Outcome ; Up-Regulation/genetics ; rac1 GTP-Binding Protein/metabolism
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Contributed Indexing:
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Keywords: AKT/mTOR; KIF18B; Lung adenocarcinoma; Prognosis; Rac1-GTP
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Substance Nomenclature:
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0 (RAC1 protein, human)
EC 2.7.1.1 (MTOR protein, human)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
EC 3.6.1.- (KIF18B protein, human)
EC 3.6.4.4 (Kinesins)
EC 3.6.5.2 (rac1 GTP-Binding Protein)
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Entry Date(s):
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Date Created: 20191125 Date Completed: 20200416 Latest Revision: 20211204
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Update Code:
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20240104
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DOI:
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10.1016/j.tice.2019.09.001
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PMID:
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31759406
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KIF18B is involved in several tumor progression and exerts critical effects on microtubule growth during mitosis, but its role in lung adenocarcinoma still remains rare. Hence, we attempted to explore the biological function of KIF18B in lung adenocarcinoma. We first analyzed the expressional pattern of KIF18B in lung adenocarcinoma, and detected the correlation between KIF18B expression and clinical characteristics in lung adenocarcinoma based on The Cancer Genome Atlas (TCGA) database and Oncomine dataset. Subsequently, cell counting kit-8 (CCK-8) assay, wound-healing analysis, and transwell method were performed to assess the effects of KIF18B in lung adenocarcinoma cells. Quantitative real-time reverse transcription-PCR (qRT-PCR) and western blotting were utilized to measure the mRNA and protein expression levels. Our results illustrated that KIF18B expression was significantly up-regulated in lung adenocarcinoma samples compared to normal specimens. High levels of KIF18B were associated with unfavorable prognosis of lung adenocarcinoma patients. Down-regulation of KIF18B in lung adenocarcinoma cells inhibited cell prolifartion, migration, and invasion. Western blot assay demonstrated that KIF18B knockdown markedly decreased Rac1-GTP expression, an important marker of migration and invasion in tumors. Moreover, the phosphorylation of AKT and mTOR expression levels were attenuated after KIF18B knockdown. Taken together, these data enhanced the point that KIF18B might promote lung adenocarcinoma cell proliferation, migration, and invasion by activating Rac1 and mediating the AKT/mTOR signaling pathway.
(Copyright © 2019 Elsevier Ltd. All rights reserved.)
