Cargando…

AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer

Prostate cancer (PCa) was one of the most commonly diagnosed malignant cancers in males in China. Cell-cycle aberration was a hallmark of cancer. SPC25, a component of Ndc80 complex, played an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in pros...

Descripción completa

Detalles Bibliográficos
Autores principales: Cui, Feilun, Hu, Jiangpeng, Tan, Jian, Tang, Huaming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5565525/
http://dx.doi.org/10.21037/tau.2017.s078
_version_ 1783258393506480128
author Cui, Feilun
Hu, Jiangpeng
Tan, Jian
Tang, Huaming
author_facet Cui, Feilun
Hu, Jiangpeng
Tan, Jian
Tang, Huaming
author_sort Cui, Feilun
collection PubMed
description Prostate cancer (PCa) was one of the most commonly diagnosed malignant cancers in males in China. Cell-cycle aberration was a hallmark of cancer. SPC25, a component of Ndc80 complex, played an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in prostate cancer were still poorly understood. Our study showed for the first time that SPC25 was significantly upregulated in prostate cancer. To explore the molecular function roles of SPC25, we performed loss of function assay and found SPC25 knockdown inhibited cell proliferation and induced the decrease in S phase and the increase in G2/M phase. Furthermore, SPC25 knockdown promoted apoptosis of prostate cancer cells. Of note, bioinformatics analysis also revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, role of tissue factor in cancer, TGF-β signaling, and sumoylation pathway in PCa. Here, we also evaluated possible prognostic value of SPC25 using TCGA RNA-seq data and we found showed SPC25 was upregulated in high pathology stage PCa. Kaplan-Meier analysis showed that Lower SPC25 expression level was associated with better survival of PCa patients. All these results suggest that SPC25 play an oncogenic role in PCa and could act as a novel diagnostic and therapeutic target for prostate cancer.
format Online
Article
Text
id pubmed-5565525
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher AME Publishing Company
record_format MEDLINE/PubMed
spelling pubmed-55655252017-09-01 AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer Cui, Feilun Hu, Jiangpeng Tan, Jian Tang, Huaming Transl Androl Urol Printed Abstracts Prostate cancer (PCa) was one of the most commonly diagnosed malignant cancers in males in China. Cell-cycle aberration was a hallmark of cancer. SPC25, a component of Ndc80 complex, played an important role in regulating mitotic chromosome segregation. However, the functional roles of SPC25 in prostate cancer were still poorly understood. Our study showed for the first time that SPC25 was significantly upregulated in prostate cancer. To explore the molecular function roles of SPC25, we performed loss of function assay and found SPC25 knockdown inhibited cell proliferation and induced the decrease in S phase and the increase in G2/M phase. Furthermore, SPC25 knockdown promoted apoptosis of prostate cancer cells. Of note, bioinformatics analysis also revealed multiple functional roles of SPC25 in regulating cell proliferation, apoptosis, invasion, role of tissue factor in cancer, TGF-β signaling, and sumoylation pathway in PCa. Here, we also evaluated possible prognostic value of SPC25 using TCGA RNA-seq data and we found showed SPC25 was upregulated in high pathology stage PCa. Kaplan-Meier analysis showed that Lower SPC25 expression level was associated with better survival of PCa patients. All these results suggest that SPC25 play an oncogenic role in PCa and could act as a novel diagnostic and therapeutic target for prostate cancer. AME Publishing Company 2017-08 /pmc/articles/PMC5565525/ http://dx.doi.org/10.21037/tau.2017.s078 Text en 2017 Translational Andrology and Urology. All rights reserved.
spellingShingle Printed Abstracts
Cui, Feilun
Hu, Jiangpeng
Tan, Jian
Tang, Huaming
AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title_full AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title_fullStr AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title_full_unstemmed AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title_short AB078. Knockdown of SPC25 inhibits cell proliferation and cycle progression in prostate cancer
title_sort ab078. knockdown of spc25 inhibits cell proliferation and cycle progression in prostate cancer
topic Printed Abstracts
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5565525/
http://dx.doi.org/10.21037/tau.2017.s078
work_keys_str_mv AT cuifeilun ab078knockdownofspc25inhibitscellproliferationandcycleprogressioninprostatecancer
AT hujiangpeng ab078knockdownofspc25inhibitscellproliferationandcycleprogressioninprostatecancer
AT tanjian ab078knockdownofspc25inhibitscellproliferationandcycleprogressioninprostatecancer
AT tanghuaming ab078knockdownofspc25inhibitscellproliferationandcycleprogressioninprostatecancer