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The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion

Purpose: Collagen type I alpha 2 chain (COL1A2) has been shown to participate in the development of various human malignancies. However, the role of COL1A2 in human colorectal cancer (CRC) remains unknown. This study investigated the expression pattern of COL1A2 in primary CRC tissues as well as the...

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Autores principales: Yu, Yifan, Liu, Dongliang, Liu, Zhenghao, Li, Shuqiang, Ge, Yang, Sun, Wei, Liu, Baolin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6096367/
https://www.ncbi.nlm.nih.gov/pubmed/30123364
http://dx.doi.org/10.7150/jca.25542
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author Yu, Yifan
Liu, Dongliang
Liu, Zhenghao
Li, Shuqiang
Ge, Yang
Sun, Wei
Liu, Baolin
author_facet Yu, Yifan
Liu, Dongliang
Liu, Zhenghao
Li, Shuqiang
Ge, Yang
Sun, Wei
Liu, Baolin
author_sort Yu, Yifan
collection PubMed
description Purpose: Collagen type I alpha 2 chain (COL1A2) has been shown to participate in the development of various human malignancies. However, the role of COL1A2 in human colorectal cancer (CRC) remains unknown. This study investigated the expression pattern of COL1A2 in primary CRC tissues as well as the correlation of COL1A2 expression with clinicopathological features and prognosis of CRC. The function of COL1A2 in CRC cell proliferation, migration, and invasion as well as the possible mechanisms were also examined. Methods: Real-time PCR and immunohistochemical analysis were performed to determine the expression of COL1A2 in primary cancer tissues and adjacent normal tissues from CRC patients. A COL1A2-expressing lentiviral vector was transfected into CRC cells, and cell counting kit-8 and Transwell assays were used to explore the effects of COL1A2 on CRC cell proliferation, migration, and invasion. Microarray-based mRNA expression profile screening was performed to reveal the possible signaling pathways involved in COL1A2-regulated cell behaviors. Results: COL1A2 was significantly downregulated in primary CRC tissues. The mRNA levels of COL1A2 in CRC tissues were correlated with tumor differentiation, invasion, and lymph node metastasis. Overexpression of COL1A2 inhibited proliferation, migration, and invasion of CRC cell lines (SW480 and SW620). The microarray analysis showed that COL1A2 overexpression regulated numerous oncogenes and cancer-related signaling pathways. Among them, altered expression of ten representative cancer-related genes in these pathways were further confirmed by western blotting. Conclusions: Our study identified COL1A2 as a novel tumor suppressor in CRC and provided a potential therapeutic approach to treat CRC.
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spelling pubmed-60963672018-08-17 The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion Yu, Yifan Liu, Dongliang Liu, Zhenghao Li, Shuqiang Ge, Yang Sun, Wei Liu, Baolin J Cancer Research Paper Purpose: Collagen type I alpha 2 chain (COL1A2) has been shown to participate in the development of various human malignancies. However, the role of COL1A2 in human colorectal cancer (CRC) remains unknown. This study investigated the expression pattern of COL1A2 in primary CRC tissues as well as the correlation of COL1A2 expression with clinicopathological features and prognosis of CRC. The function of COL1A2 in CRC cell proliferation, migration, and invasion as well as the possible mechanisms were also examined. Methods: Real-time PCR and immunohistochemical analysis were performed to determine the expression of COL1A2 in primary cancer tissues and adjacent normal tissues from CRC patients. A COL1A2-expressing lentiviral vector was transfected into CRC cells, and cell counting kit-8 and Transwell assays were used to explore the effects of COL1A2 on CRC cell proliferation, migration, and invasion. Microarray-based mRNA expression profile screening was performed to reveal the possible signaling pathways involved in COL1A2-regulated cell behaviors. Results: COL1A2 was significantly downregulated in primary CRC tissues. The mRNA levels of COL1A2 in CRC tissues were correlated with tumor differentiation, invasion, and lymph node metastasis. Overexpression of COL1A2 inhibited proliferation, migration, and invasion of CRC cell lines (SW480 and SW620). The microarray analysis showed that COL1A2 overexpression regulated numerous oncogenes and cancer-related signaling pathways. Among them, altered expression of ten representative cancer-related genes in these pathways were further confirmed by western blotting. Conclusions: Our study identified COL1A2 as a novel tumor suppressor in CRC and provided a potential therapeutic approach to treat CRC. Ivyspring International Publisher 2018-07-30 /pmc/articles/PMC6096367/ /pubmed/30123364 http://dx.doi.org/10.7150/jca.25542 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Yu, Yifan
Liu, Dongliang
Liu, Zhenghao
Li, Shuqiang
Ge, Yang
Sun, Wei
Liu, Baolin
The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title_full The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title_fullStr The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title_full_unstemmed The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title_short The inhibitory effects of COL1A2 on colorectal cancer cell proliferation, migration, and invasion
title_sort inhibitory effects of col1a2 on colorectal cancer cell proliferation, migration, and invasion
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6096367/
https://www.ncbi.nlm.nih.gov/pubmed/30123364
http://dx.doi.org/10.7150/jca.25542
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