CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.

Human CMTM3 has been proposed as a putative tumor suppressor gene. The loss of CMTM3 has been found in several carcinomas. However, the regulation of CMTM3 expression and its function in tumor progression remain largely unknown. Here, we investigated the regulation of CMTM3 expression, function and...

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Autores principales: Zesong Li, Jun Xie, Jianting Wu, Wenjie Li, Liping Nie, Xiaojuan Sun, Aifa Tang, Xianxin Li, Ren Liu, Hongbing Mei, Feng Wang, Zhiping Wang, Yaoting Gui, Zhiming Cai
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Publicado: Public Library of Science (PLoS) 2014
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Acceso en línea:https://doaj.org/article/738e4ccadeed45e9b2705ec332035bbc
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spelling oai:doaj.org-article:738e4ccadeed45e9b2705ec332035bbc2021-11-18T08:30:34ZCMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.1932-620310.1371/journal.pone.0088965https://doaj.org/article/738e4ccadeed45e9b2705ec332035bbc2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24586462/?tool=EBIhttps://doaj.org/toc/1932-6203Human CMTM3 has been proposed as a putative tumor suppressor gene. The loss of CMTM3 has been found in several carcinomas. However, the regulation of CMTM3 expression and its function in tumor progression remain largely unknown. Here, we investigated the regulation of CMTM3 expression, function and molecular mechanism in human testicular cancer cells. CMTM3 was frequently downregulated or silenced in testicular cancer cell lines and tumor tissues but highly expressed in normal testis tissues. The re-expression of CMTM3 significantly suppressed the colony formation, proliferation, and migration capacity of testicular cancer cells by inducing a G2 cell cycle arrest and apoptosis. Moreover, the re-expression of CMTM3 activated the transcription of p53, induced p53 accumulation, up-regulated the expression of p21, and increased the cleavage of caspase 9, 8, 3, and PARP. The downregulation of CMTM3 in clinical tumor tissues was associated with the methylation of a single CpG site located within the Sp1/Sp3-responsive region of the core promoter. These results indicate that CMTM3 can function as tumor suppressor through the induction of a G2 cell cycle arrest and apoptosis. CMTM3 is thus involved in testicular cancer pathogenesis, and it is frequently at least partially silenced by the methylation of a single, specific CpG site in tumor tissues.Zesong LiJun XieJianting WuWenjie LiLiping NieXiaojuan SunAifa TangXianxin LiRen LiuHongbing MeiFeng WangZhiping WangYaoting GuiZhiming CaiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 2, p e88965 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Zesong Li
Jun Xie
Jianting Wu
Wenjie Li
Liping Nie
Xiaojuan Sun
Aifa Tang
Xianxin Li
Ren Liu
Hongbing Mei
Feng Wang
Zhiping Wang
Yaoting Gui
Zhiming Cai
CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
description Human CMTM3 has been proposed as a putative tumor suppressor gene. The loss of CMTM3 has been found in several carcinomas. However, the regulation of CMTM3 expression and its function in tumor progression remain largely unknown. Here, we investigated the regulation of CMTM3 expression, function and molecular mechanism in human testicular cancer cells. CMTM3 was frequently downregulated or silenced in testicular cancer cell lines and tumor tissues but highly expressed in normal testis tissues. The re-expression of CMTM3 significantly suppressed the colony formation, proliferation, and migration capacity of testicular cancer cells by inducing a G2 cell cycle arrest and apoptosis. Moreover, the re-expression of CMTM3 activated the transcription of p53, induced p53 accumulation, up-regulated the expression of p21, and increased the cleavage of caspase 9, 8, 3, and PARP. The downregulation of CMTM3 in clinical tumor tissues was associated with the methylation of a single CpG site located within the Sp1/Sp3-responsive region of the core promoter. These results indicate that CMTM3 can function as tumor suppressor through the induction of a G2 cell cycle arrest and apoptosis. CMTM3 is thus involved in testicular cancer pathogenesis, and it is frequently at least partially silenced by the methylation of a single, specific CpG site in tumor tissues.
format article
author Zesong Li
Jun Xie
Jianting Wu
Wenjie Li
Liping Nie
Xiaojuan Sun
Aifa Tang
Xianxin Li
Ren Liu
Hongbing Mei
Feng Wang
Zhiping Wang
Yaoting Gui
Zhiming Cai
author_facet Zesong Li
Jun Xie
Jianting Wu
Wenjie Li
Liping Nie
Xiaojuan Sun
Aifa Tang
Xianxin Li
Ren Liu
Hongbing Mei
Feng Wang
Zhiping Wang
Yaoting Gui
Zhiming Cai
author_sort Zesong Li
title CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
title_short CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
title_full CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
title_fullStr CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
title_full_unstemmed CMTM3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
title_sort cmtm3 inhibits human testicular cancer cell growth through inducing cell-cycle arrest and apoptosis.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/738e4ccadeed45e9b2705ec332035bbc
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