Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest

Rong Xie,* Yichao Zhang,* Chao Shen, Xiaoyun Cao, Shixin Gu,* Xiaoming Che*Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China *These authors contributed equally to this work Abstract: “Glioblastoma multiforme” (GBM) is t...

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Main Authors: Xie R, Zhang YC, Shen C, Cao XY, Gu SX, Che XM
Format: Article
Language:English
Published: Dove Medical Press 2015-05-01
Series:OncoTargets and Therapy
Online Access:http://www.dovepress.com/knockdown-of-immature-colon-carcinoma-transcript-1-inhibits-proliferat-peer-reviewed-article-OTT
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spelling doaj-cc9b96a9241547bc85c36c9a48ae5b162020-11-24T21:26:31ZengDove Medical PressOncoTargets and Therapy1178-69302015-05-012015default1119112721794Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrestXie RZhang YCShen CCao XYGu SXChe XMRong Xie,* Yichao Zhang,* Chao Shen, Xiaoyun Cao, Shixin Gu,* Xiaoming Che*Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China *These authors contributed equally to this work Abstract: “Glioblastoma multiforme” (GBM) is the frequent form of malignant glioma. Immature colon carcinoma transcript-1 (ICT1) is essential for cell vitality and mitochondrial function and has been recognized in several human cancers. In the study reported here, we attempted to evaluate the functional role of ICT1 in GBM cells. Lentivirus-mediated RNA interference (RNAi) was applied to silence ICT1 expression in human GBM cell lines U251 and U87. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony-formation assays. Cell-cycle progression was determined by flow cytometry with propidium iodide staining. The results revealed that lentivirus-mediated short hairpin RNA (shRNA) can specifically suppress the expression of ICT1 in U251 and U87 cells. Functional investigations proved for the first time, as far as we are aware, that ICT1 knockdown significantly inhibited the proliferation of both cell lines. Moreover, the cell cycle of U251 cells was arrested at Gap 2 (G2)/mitotic (M) phase after ICT1 knockdown, with a concomitant accumulation of cells in the Sub-Gap 1 (G1) phase. This study highlights the crucial role of ICT1 in promoting GBM cell proliferation, and provides a foundation for further study into the clinical potential of lentivirus-mediated silencing of ICT1 for GBM therapy. Keywords: glioblastoma multiforme, immature colon carcinoma transcript-1, lentivirus, proliferation, RNA interferencehttp://www.dovepress.com/knockdown-of-immature-colon-carcinoma-transcript-1-inhibits-proliferat-peer-reviewed-article-OTT
collection DOAJ
language English
format Article
sources DOAJ
author Xie R
Zhang YC
Shen C
Cao XY
Gu SX
Che XM
spellingShingle Xie R
Zhang YC
Shen C
Cao XY
Gu SX
Che XM
Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
OncoTargets and Therapy
author_facet Xie R
Zhang YC
Shen C
Cao XY
Gu SX
Che XM
author_sort Xie R
title Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
title_short Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
title_full Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
title_fullStr Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
title_full_unstemmed Knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through Gap 2/mitotic phase arrest
title_sort knockdown of immature colon carcinoma transcript-1 inhibits proliferation of glioblastoma multiforme cells through gap 2/mitotic phase arrest
publisher Dove Medical Press
series OncoTargets and Therapy
issn 1178-6930
publishDate 2015-05-01
description Rong Xie,* Yichao Zhang,* Chao Shen, Xiaoyun Cao, Shixin Gu,* Xiaoming Che*Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China *These authors contributed equally to this work Abstract: “Glioblastoma multiforme” (GBM) is the frequent form of malignant glioma. Immature colon carcinoma transcript-1 (ICT1) is essential for cell vitality and mitochondrial function and has been recognized in several human cancers. In the study reported here, we attempted to evaluate the functional role of ICT1 in GBM cells. Lentivirus-mediated RNA interference (RNAi) was applied to silence ICT1 expression in human GBM cell lines U251 and U87. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony-formation assays. Cell-cycle progression was determined by flow cytometry with propidium iodide staining. The results revealed that lentivirus-mediated short hairpin RNA (shRNA) can specifically suppress the expression of ICT1 in U251 and U87 cells. Functional investigations proved for the first time, as far as we are aware, that ICT1 knockdown significantly inhibited the proliferation of both cell lines. Moreover, the cell cycle of U251 cells was arrested at Gap 2 (G2)/mitotic (M) phase after ICT1 knockdown, with a concomitant accumulation of cells in the Sub-Gap 1 (G1) phase. This study highlights the crucial role of ICT1 in promoting GBM cell proliferation, and provides a foundation for further study into the clinical potential of lentivirus-mediated silencing of ICT1 for GBM therapy. Keywords: glioblastoma multiforme, immature colon carcinoma transcript-1, lentivirus, proliferation, RNA interference
url http://www.dovepress.com/knockdown-of-immature-colon-carcinoma-transcript-1-inhibits-proliferat-peer-reviewed-article-OTT
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