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Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis

Emerging evidence shows that exocytosis plays a key role in tumor development and metastasis. Secernin-1 (SCRN1) is a novel regulator of exocytosis. Our previous work identified SCRN1 as a tumor-associated gene by bioinformatics analysis of transcriptomes. In this study, we demonstrated the aberrant...

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Autores principales: Lin, Shengtao, Jiang, Tao, Yu, Yang, Tang, Huamei, Lu, Su, Peng, Zhihai, Fan, Junwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357136/
https://www.ncbi.nlm.nih.gov/pubmed/25814779
http://dx.doi.org/10.1155/2015/230703
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author Lin, Shengtao
Jiang, Tao
Yu, Yang
Tang, Huamei
Lu, Su
Peng, Zhihai
Fan, Junwei
author_facet Lin, Shengtao
Jiang, Tao
Yu, Yang
Tang, Huamei
Lu, Su
Peng, Zhihai
Fan, Junwei
author_sort Lin, Shengtao
collection PubMed
description Emerging evidence shows that exocytosis plays a key role in tumor development and metastasis. Secernin-1 (SCRN1) is a novel regulator of exocytosis. Our previous work identified SCRN1 as a tumor-associated gene by bioinformatics analysis of transcriptomes. In this study, we demonstrated the aberrant overexpression of SCRN1 at mRNA and protein level in colon cancer. We also revealed that overexpression of SCRN1 was significantly associated with the tumor development and poor prognosis. Experiments in vitro validated that SCRN1 may promote cancer cell proliferation and secretion of matrix metalloproteinase-2/9 (MMP-2/9) proteins to accelerate tumor progression.
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spelling pubmed-43571362015-03-26 Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis Lin, Shengtao Jiang, Tao Yu, Yang Tang, Huamei Lu, Su Peng, Zhihai Fan, Junwei Dis Markers Research Article Emerging evidence shows that exocytosis plays a key role in tumor development and metastasis. Secernin-1 (SCRN1) is a novel regulator of exocytosis. Our previous work identified SCRN1 as a tumor-associated gene by bioinformatics analysis of transcriptomes. In this study, we demonstrated the aberrant overexpression of SCRN1 at mRNA and protein level in colon cancer. We also revealed that overexpression of SCRN1 was significantly associated with the tumor development and poor prognosis. Experiments in vitro validated that SCRN1 may promote cancer cell proliferation and secretion of matrix metalloproteinase-2/9 (MMP-2/9) proteins to accelerate tumor progression. Hindawi Publishing Corporation 2015 2015-02-26 /pmc/articles/PMC4357136/ /pubmed/25814779 http://dx.doi.org/10.1155/2015/230703 Text en Copyright © 2015 Shengtao Lin et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Lin, Shengtao
Jiang, Tao
Yu, Yang
Tang, Huamei
Lu, Su
Peng, Zhihai
Fan, Junwei
Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title_full Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title_fullStr Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title_full_unstemmed Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title_short Secernin-1 Contributes to Colon Cancer Progression through Enhancing Matrix Metalloproteinase-2/9 Exocytosis
title_sort secernin-1 contributes to colon cancer progression through enhancing matrix metalloproteinase-2/9 exocytosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357136/
https://www.ncbi.nlm.nih.gov/pubmed/25814779
http://dx.doi.org/10.1155/2015/230703
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