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Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression

T cell immunoglobulin mucin-3 (Tim-3) has previously been implicated in the immune response and tumor biology. Colorectal carcinoma (CRC) is a malignancy, which is closely associated with inflammation. However, the role of Tim-3 in the progression of CRC remains to be fully elucidated. The present s...

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Autores principales: Yu, Muming, Lu, Bin, Liu, Yancun, Me, Ying, Wang, Lijun, Zhang, Peng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364832/
https://www.ncbi.nlm.nih.gov/pubmed/28035413
http://dx.doi.org/10.3892/mmr.2016.6065
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author Yu, Muming
Lu, Bin
Liu, Yancun
Me, Ying
Wang, Lijun
Zhang, Peng
author_facet Yu, Muming
Lu, Bin
Liu, Yancun
Me, Ying
Wang, Lijun
Zhang, Peng
author_sort Yu, Muming
collection PubMed
description T cell immunoglobulin mucin-3 (Tim-3) has previously been implicated in the immune response and tumor biology. Colorectal carcinoma (CRC) is a malignancy, which is closely associated with inflammation. However, the role of Tim-3 in the progression of CRC remains to be fully elucidated. The present study aimed to investigate the role of Tim-3 in the progressive activities of human CRC. A total of 30 clinical CRC tissues and their adjacent tissues were collected. Slides from another 112 cases that underwent CRC surgical resection were also obtained. The protein and mRNA levels of Tim-3 in the clinical tissues and in CRC cell lines were initially examined using western blot and reverse transcription-quantitative polymerase chain reaction analyses, respectively. Immunohistochemical staining was performed to detect Tim-3 in the CRC samples. Specific small interfering (si)RNA against Tim-3 (siTim-3) was synthesized to knock down the expression of Tim-3, and the subsequent effects of Tim-3 knockdown on cell proliferation, migration and invasion were assessed. The data obtained showed that Tim-3 was expressed at high levels in the CRC tissues, compared with the non-cancerous tissues. The expression of Tim-3 in the clinical tissues was significantly associated with tumor size (P=0.007), tumor-node-metastasis staging (P<0.0001) and distant metastasis (P<0.0001). Knockdown of Tim-3 significantly reduced the cell proliferative rate of HCT116 and HT-29 cells. Wound closure activity was also inhibited by knockdown of Tim-3 in these two cell lines, and the migration and invasive abilities of these two cell lines were consistently decreased following knockdown of Tim-3. Taken together, Tim-3 was found to be a critical mediator in the progression of CRC and may serve as a potential therapeutic target for the treatment of CRC.
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spelling pubmed-53648322017-05-15 Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression Yu, Muming Lu, Bin Liu, Yancun Me, Ying Wang, Lijun Zhang, Peng Mol Med Rep Articles T cell immunoglobulin mucin-3 (Tim-3) has previously been implicated in the immune response and tumor biology. Colorectal carcinoma (CRC) is a malignancy, which is closely associated with inflammation. However, the role of Tim-3 in the progression of CRC remains to be fully elucidated. The present study aimed to investigate the role of Tim-3 in the progressive activities of human CRC. A total of 30 clinical CRC tissues and their adjacent tissues were collected. Slides from another 112 cases that underwent CRC surgical resection were also obtained. The protein and mRNA levels of Tim-3 in the clinical tissues and in CRC cell lines were initially examined using western blot and reverse transcription-quantitative polymerase chain reaction analyses, respectively. Immunohistochemical staining was performed to detect Tim-3 in the CRC samples. Specific small interfering (si)RNA against Tim-3 (siTim-3) was synthesized to knock down the expression of Tim-3, and the subsequent effects of Tim-3 knockdown on cell proliferation, migration and invasion were assessed. The data obtained showed that Tim-3 was expressed at high levels in the CRC tissues, compared with the non-cancerous tissues. The expression of Tim-3 in the clinical tissues was significantly associated with tumor size (P=0.007), tumor-node-metastasis staging (P<0.0001) and distant metastasis (P<0.0001). Knockdown of Tim-3 significantly reduced the cell proliferative rate of HCT116 and HT-29 cells. Wound closure activity was also inhibited by knockdown of Tim-3 in these two cell lines, and the migration and invasive abilities of these two cell lines were consistently decreased following knockdown of Tim-3. Taken together, Tim-3 was found to be a critical mediator in the progression of CRC and may serve as a potential therapeutic target for the treatment of CRC. D.A. Spandidos 2017-02 2016-12-22 /pmc/articles/PMC5364832/ /pubmed/28035413 http://dx.doi.org/10.3892/mmr.2016.6065 Text en Copyright: © Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Yu, Muming
Lu, Bin
Liu, Yancun
Me, Ying
Wang, Lijun
Zhang, Peng
Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title_full Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title_fullStr Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title_full_unstemmed Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title_short Tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
title_sort tim-3 is upregulated in human colorectal carcinoma and associated with tumor progression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364832/
https://www.ncbi.nlm.nih.gov/pubmed/28035413
http://dx.doi.org/10.3892/mmr.2016.6065
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