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Erschienen in: Tumor Biology 3/2016

21.10.2015 | Original Article

Expression of CDC5L is associated with tumor progression in gliomas

verfasst von: Wenjuan Chen, Li Zhang, Yan Wang, Jie Sun, Donglin Wang, Shaochen Fan, Na Ban, Junya Zhu, Bin Ji, Yuchan Wang

Erschienen in: Tumor Biology | Ausgabe 3/2016

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Abstract

Cell division cycle 5-like (CDC5L) protein is a cell cycle regulator of the G2/M transition and has been reported to participate in the catalytic step of pre-messenger RNA (mRNA) splicing and DNA damage repair. Recently, it was also found to act as a candidate oncogene in osteosarcoma and cervical tumors. However, the role of CDC5L expression in tumor biology was still unclear. Here, we analyzed the expression and clinical significance of CDC5L in gliomas. The expression of CDC5L in fresh glioma tissues and paraffin-embedded slices was evaluated by western blot and immunohistochemistry, respectively. We found that CDC5L was highly expressed in glioma tissues. The expression of CDC5L was significantly associated with glioma pathology grade and Ki-67 expression. Univariate and multivariate analyses showed that high CDC5L expression was an independent prognostic factor for glioma patients’ survival. To determine whether CDC5L could regulate the proliferation of glioma cells, we transfected glioma cells with interfering RNA target CDC5L, then investigated cell proliferation with cell counting kit (CCK)-8, flow cytometry assays and colony formation analyses. Our results indicated that knockdown of CDC5L would inhibit proliferation of glioma cells. Besides, reduced expression of CDC5L could induce the apoptosis of glioma cells. These findings suggested that CDC5L might play an important role in glioma and thus be a promising therapeutic target of glioma.
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Metadaten
Titel
Expression of CDC5L is associated with tumor progression in gliomas
verfasst von
Wenjuan Chen
Li Zhang
Yan Wang
Jie Sun
Donglin Wang
Shaochen Fan
Na Ban
Junya Zhu
Bin Ji
Yuchan Wang
Publikationsdatum
21.10.2015
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 3/2016
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4088-5

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