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Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer

Prostate cancer (PCa) is the most frequently diagnosed type of cancer in Chinese males. Cell-cycle aberration is a hallmark of cancer. Spindle pole body component 25 homolog (SPC25), a component of the Ndc80 complex, serves an important role in regulating mitotic chromosome segregation. However, the...

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Autores principales: Cui, Feilun, Hu, Jianpeng, Fan, Yu, Tan, Jian, Tang, Huaming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840511/
https://www.ncbi.nlm.nih.gov/pubmed/29552205
http://dx.doi.org/10.3892/ol.2018.8003
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author Cui, Feilun
Hu, Jianpeng
Fan, Yu
Tan, Jian
Tang, Huaming
author_facet Cui, Feilun
Hu, Jianpeng
Fan, Yu
Tan, Jian
Tang, Huaming
author_sort Cui, Feilun
collection PubMed
description Prostate cancer (PCa) is the most frequently diagnosed type of cancer in Chinese males. Cell-cycle aberration is a hallmark of cancer. Spindle pole body component 25 homolog (SPC25), a component of the Ndc80 complex, serves an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in PCa remain poorly understood. To the best of our knowledge, the present study was the first to demonstrate that SPC25 is significantly upregulated in PCa. In order to investigate the molecular roles of SPC25, a loss of function assay was performed, revealing that SPC25 knockdown inhibited cell proliferation, and induced a decrease in the number of cells in the S phase and an increase in the number of cells in the G2/M phase. Furthermore, SPC25 knockdown promoted the apoptosis of PCa cells. Additionally, bioinformatics analysis revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, transforming growth factor-β signaling and the SUMOylation pathway in PCa. The present study also evaluated the potential prognostic value of SPC25 using The Cancer Genome Atlas RNA-seq data and demonstrated that SPC25 was upregulated in late stage PCa. Kaplan-Meier analysis demonstrated that lower SPC25 expression was associated with an improved survival rate in patients with PCa. Taken together, these results suggested that SPC25 serves an oncogenic role in PCa and may act as a novel diagnostic and therapeutic target for PCa.
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spelling pubmed-58405112018-03-16 Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer Cui, Feilun Hu, Jianpeng Fan, Yu Tan, Jian Tang, Huaming Oncol Lett Articles Prostate cancer (PCa) is the most frequently diagnosed type of cancer in Chinese males. Cell-cycle aberration is a hallmark of cancer. Spindle pole body component 25 homolog (SPC25), a component of the Ndc80 complex, serves an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in PCa remain poorly understood. To the best of our knowledge, the present study was the first to demonstrate that SPC25 is significantly upregulated in PCa. In order to investigate the molecular roles of SPC25, a loss of function assay was performed, revealing that SPC25 knockdown inhibited cell proliferation, and induced a decrease in the number of cells in the S phase and an increase in the number of cells in the G2/M phase. Furthermore, SPC25 knockdown promoted the apoptosis of PCa cells. Additionally, bioinformatics analysis revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, transforming growth factor-β signaling and the SUMOylation pathway in PCa. The present study also evaluated the potential prognostic value of SPC25 using The Cancer Genome Atlas RNA-seq data and demonstrated that SPC25 was upregulated in late stage PCa. Kaplan-Meier analysis demonstrated that lower SPC25 expression was associated with an improved survival rate in patients with PCa. Taken together, these results suggested that SPC25 serves an oncogenic role in PCa and may act as a novel diagnostic and therapeutic target for PCa. D.A. Spandidos 2018-04 2018-02-08 /pmc/articles/PMC5840511/ /pubmed/29552205 http://dx.doi.org/10.3892/ol.2018.8003 Text en Copyright: © Cui et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Cui, Feilun
Hu, Jianpeng
Fan, Yu
Tan, Jian
Tang, Huaming
Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title_full Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title_fullStr Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title_full_unstemmed Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title_short Knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
title_sort knockdown of spindle pole body component 25 homolog inhibits cell proliferation and cycle progression in prostate cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840511/
https://www.ncbi.nlm.nih.gov/pubmed/29552205
http://dx.doi.org/10.3892/ol.2018.8003
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