Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy

Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and β-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear β-catenin through restraining β-catenin from cytoplasm into nuclei or it could also promote β-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.

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Main Authors: Wang,Z.K., Yang,L., Wu,L.L., Mao,H., Zhou,Y.H., Zhang,P.F., Dai,G.H.
Format: Digital revista
Language:English
Published: Associação Brasileira de Divulgação Científica 2018
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000200607
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spelling oai:scielo:S0100-879X20180002006072019-03-19Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapyWang,Z.K.Yang,L.Wu,L.L.Mao,H.Zhou,Y.H.Zhang,P.F.Dai,G.H. Colon cancer LINC00261 β-catenin Cisplatin resistance Mechanism Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and β-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear β-catenin through restraining β-catenin from cytoplasm into nuclei or it could also promote β-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.info:eu-repo/semantics/openAccessAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research v.51 n.2 20182018-01-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000200607en10.1590/1414-431x20176793
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country Brasil
countrycode BR
component Revista
access En linea
databasecode rev-scielo-br
tag revista
region America del Sur
libraryname SciELO
language English
format Digital
author Wang,Z.K.
Yang,L.
Wu,L.L.
Mao,H.
Zhou,Y.H.
Zhang,P.F.
Dai,G.H.
spellingShingle Wang,Z.K.
Yang,L.
Wu,L.L.
Mao,H.
Zhou,Y.H.
Zhang,P.F.
Dai,G.H.
Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
author_facet Wang,Z.K.
Yang,L.
Wu,L.L.
Mao,H.
Zhou,Y.H.
Zhang,P.F.
Dai,G.H.
author_sort Wang,Z.K.
title Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
title_short Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
title_full Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
title_fullStr Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
title_full_unstemmed Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy
title_sort long non-coding rna linc00261 sensitizes human colon cancer cells to cisplatin therapy
description Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and β-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear β-catenin through restraining β-catenin from cytoplasm into nuclei or it could also promote β-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
publisher Associação Brasileira de Divulgação Científica
publishDate 2018
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000200607
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