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CCDC34 is up-regulated in bladder cancer and regulates bladder cancer cell proliferation, apoptosis and migration

The coiled coil is a superhelical structural protein motif involved in a diverse array of biological functions, and the abnormal expression of the coiled-coil domain containing proteins has a direct link with the phenotype of tumor cell migration, invasion and metastasis. The aim of this study was t... Full description

Journal Title: Oncotarget 22 September 2015, Vol.6(28), pp.25856-67
Main Author: Gong, Yanqing
Other Authors: Qiu, Wei , Ning, Xianghui , Yang, Xinyu , Liu, Libo , Wang, Zicheng , Lin, Jian , Li, Xuesong , Guo, Yinglu
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1949-2553 ; PMID: 26312564 Version:1 ; DOI: 10.18632/oncotarget.4624
Link: http://pubmed.gov/26312564
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recordid: medline26312564
title: CCDC34 is up-regulated in bladder cancer and regulates bladder cancer cell proliferation, apoptosis and migration
format: Article
creator:
  • Gong, Yanqing
  • Qiu, Wei
  • Ning, Xianghui
  • Yang, Xinyu
  • Liu, Libo
  • Wang, Zicheng
  • Lin, Jian
  • Li, Xuesong
  • Guo, Yinglu
subjects:
  • Ccdc34
  • Bladder Cancer
  • Migration
  • Proliferation
  • Sirna
  • Apoptosis
  • Cell Movement
  • Cell Proliferation
  • Antigens, Neoplasm -- Metabolism
  • Neoplasm Proteins -- Metabolism
  • Urinary Bladder Neoplasms -- Metabolism
ispartof: Oncotarget, 22 September 2015, Vol.6(28), pp.25856-67
description: The coiled coil is a superhelical structural protein motif involved in a diverse array of biological functions, and the abnormal expression of the coiled-coil domain containing proteins has a direct link with the phenotype of tumor cell migration, invasion and metastasis. The aim of this study was to investigate the critical role of Coiled-coil domain-containing protein 34 (CCDC34) in bladder carcinogenesis, which has never been reported to date. Here, we found CCDC34 expression was elevated in bladder cancer tissues and cell lines. The knockdown of CCDC34 via lentivirus-mediated siRNA significantly suppressed bladder cancer cells proliferation and migration, and induced cell cycle arrest at G2/M phase and increased apoptosis in vitro. In addition, CCDC34 knockdown suppressed bladder tumor growth in nude mice. Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration. Our findings revealed for the first time a potential oncogenic role for CCDC34 in bladder carcinoma pathogenesis and it may serve as a biomarker or even a therapeutic target for bladder cancer.
language: eng
source:
identifier: E-ISSN: 1949-2553 ; PMID: 26312564 Version:1 ; DOI: 10.18632/oncotarget.4624
fulltext: fulltext
issn:
  • 19492553
  • 1949-2553
url: Link


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titleCCDC34 is up-regulated in bladder cancer and regulates bladder cancer cell proliferation, apoptosis and migration
creatorGong, Yanqing ; Qiu, Wei ; Ning, Xianghui ; Yang, Xinyu ; Liu, Libo ; Wang, Zicheng ; Lin, Jian ; Li, Xuesong ; Guo, Yinglu
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subjectCcdc34 ; Bladder Cancer ; Migration ; Proliferation ; Sirna ; Apoptosis ; Cell Movement ; Cell Proliferation ; Antigens, Neoplasm -- Metabolism ; Neoplasm Proteins -- Metabolism ; Urinary Bladder Neoplasms -- Metabolism
descriptionThe coiled coil is a superhelical structural protein motif involved in a diverse array of biological functions, and the abnormal expression of the coiled-coil domain containing proteins has a direct link with the phenotype of tumor cell migration, invasion and metastasis. The aim of this study was to investigate the critical role of Coiled-coil domain-containing protein 34 (CCDC34) in bladder carcinogenesis, which has never been reported to date. Here, we found CCDC34 expression was elevated in bladder cancer tissues and cell lines. The knockdown of CCDC34 via lentivirus-mediated siRNA significantly suppressed bladder cancer cells proliferation and migration, and induced cell cycle arrest at G2/M phase and increased apoptosis in vitro. In addition, CCDC34 knockdown suppressed bladder tumor growth in nude mice. Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration. Our findings revealed for the first time a potential oncogenic role for CCDC34 in bladder carcinoma pathogenesis and it may serve as a biomarker or even a therapeutic target for bladder cancer.
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titleCCDC34 is up-regulated in bladder cancer and regulates bladder cancer cell proliferation, apoptosis and migration
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abstractThe coiled coil is a superhelical structural protein motif involved in a diverse array of biological functions, and the abnormal expression of the coiled-coil domain containing proteins has a direct link with the phenotype of tumor cell migration, invasion and metastasis. The aim of this study was to investigate the critical role of Coiled-coil domain-containing protein 34 (CCDC34) in bladder carcinogenesis, which has never been reported to date. Here, we found CCDC34 expression was elevated in bladder cancer tissues and cell lines. The knockdown of CCDC34 via lentivirus-mediated siRNA significantly suppressed bladder cancer cells proliferation and migration, and induced cell cycle arrest at G2/M phase and increased apoptosis in vitro. In addition, CCDC34 knockdown suppressed bladder tumor growth in nude mice. Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration. Our findings revealed for the first time a potential oncogenic role for CCDC34 in bladder carcinoma pathogenesis and it may serve as a biomarker or even a therapeutic target for bladder cancer.
doi10.18632/oncotarget.4624
pmid26312564
oafree_for_read
date2015-09-22