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Tytuł pozycji:

CKAP2L Knockdown Exerts Antitumor Effects by Increasing miR-4496 in Glioblastoma Cell Lines.

Tytuł:
CKAP2L Knockdown Exerts Antitumor Effects by Increasing miR-4496 in Glioblastoma Cell Lines.
Autorzy:
Li YF; Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.
Tsai WC; Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.
Chou CH; Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 11490, Taiwan.
Huang LC; Department of Biochemistry, National Defense Medical Center, Taipei 11490, Taiwan.
Huang SM; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 11490, Taiwan.; Department of Biochemistry, National Defense Medical Center, Taipei 11490, Taiwan.
Hueng DY; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 11490, Taiwan.; Department of Biochemistry, National Defense Medical Center, Taipei 11490, Taiwan.; Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.
Tsai CK; Department of Neurology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.
Źródło:
International journal of molecular sciences [Int J Mol Sci] 2020 Dec 27; Vol. 22 (1). Date of Electronic Publication: 2020 Dec 27.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:
Brain Neoplasms/*metabolism
Cell Proliferation/*genetics
Cytoskeletal Proteins/*metabolism
Epithelial-Mesenchymal Transition/*genetics
G2 Phase Cell Cycle Checkpoints/*genetics
Gene Expression Regulation, Neoplastic/*genetics
Glioblastoma/*metabolism
MicroRNAs/*metabolism
Brain Neoplasms/genetics ; Brain Neoplasms/mortality ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement/genetics ; Central Nervous System Neoplasms/genetics ; Central Nervous System Neoplasms/metabolism ; Central Nervous System Neoplasms/mortality ; Central Nervous System Neoplasms/pathology ; Cytoskeletal Proteins/genetics ; Databases, Genetic ; E2F Transcription Factors/genetics ; E2F Transcription Factors/metabolism ; Female ; Gene Knockdown Techniques ; Glioblastoma/genetics ; Glioma/genetics ; Glioma/metabolism ; Glioma/mortality ; Glioma/pathology ; Humans ; Immunohistochemistry ; Male ; MicroRNAs/genetics ; Middle Aged ; Neoplasm Grading ; Neoplasm Invasiveness/genetics ; Prognosis ; Tissue Array Analysis
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Grant Information:
108-2314-B-016-024 Ministry of Science and Technology, Taiwan; MAB-108-064 Ministry of National Defense Medical Affairs Bureau; TSGH-C108-101 Tri-Service General Hospital; TSGH-E-109227 Tri-Service General Hospital; TSGH-D-109203 Tri-Service General Hospital
Contributed Indexing:
Keywords: CGGA; CKAP2L; TCGA; UCSC Xena; glioblastoma; glioma; miR-4496; prognosis
Substance Nomenclature:
0 (CKAP2 protein, human)
0 (Cytoskeletal Proteins)
0 (E2F Transcription Factors)
0 (MIRN4496 microRNA, human)
0 (MicroRNAs)
Entry Date(s):
Date Created: 20201230 Date Completed: 20210331 Latest Revision: 20210331
Update Code:
20240105
PubMed Central ID:
PMC7796349
DOI:
10.3390/ijms22010197
PMID:
33375517
Czasopismo naukowe
Despite advances in the diagnosis and treatment of the central nervous system malignancy glioma, overall survival remains poor. Cytoskeleton-associated protein 2-like ( CKAP2L ), which plays key roles in neural progenitor cell division, has also been linked to poor prognosis in lung cancer. In the present study, we investigated the role of CKAP2L in glioma. From bioinformatics analyses of datasets from The Cancer Gene Atlas and the Chinese Glioma Genome Atlas, we found that CKAP2L expression correlates with tumor grade and overall survival. Gene set enrichment analysis (GSEA) showed that MITOTIC_SPINDLE, G2M_CHECKPOINT, and E2F_TARGETS are crucially enriched phenotypes associated with high CKAP2L expression. Using U87MG, U118MG, and LNZ308 human glioma cells, we confirmed that CKAP2L knockdown with si CKAP2L inhibits glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Interestingly, CKAP2L knockdown also induced cell cycle arrest at G2/M phase, which is consistent with the GSEA finding. Finally, we observed that CKAP2L knockdown led to significant increases in miR-4496. Treating cells with exogenous miR-4496 mimicked the effect of CKAP2L knockdown, and the effects of CKAP2L knockdown could be suppressed by miR-4496 inhibition. These findings suggest that CKAP2L is a vital regulator of miR-4496 activity and that CKAP2L is a potentially useful prognostic marker in glioma.
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