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Down‐regulation of FN1 inhibits colorectal carcinogenesis by suppressing proliferation, migration and invasion


Fibronectin 1 (FN1) is involved in cell adhesion and migration processes including embryogenesis, wound healing, blood coagulation, host defense, metastasis and implicated in various biochemical processes. However, its effects on the development and progression of human cancer, especially colorectal cancer (CRC), are unclear. To evaluate the relationship between the expression of FN1 and the histopathologic parameters of patients with CRC or the proliferation, migration and invasion of colorectal cancer cell lines, we screened FN1 as a new candidate gene which promotes development of CRC, in an independent dataset (The Human Protein Atlas website). Here, we reported that FN1 was elevated in CRC tissues compared with normal colon tissues. Further, FN1 expression level was correlated with age, lymph vascular invasion and survival rate. Knockdown of FN1 in two CRC cell lines, LOVO and SW1116, significantly inhibited cell proliferation, migration and invasion and induced cell apoptosis. Western blot analysis showed that down‐regulation of FN1 significantly decreased the expression of Bcl‐2, MMP‐9, Twist and increased the expression of Bax, Caspase‐3 and E‐cadherin in LOVO and SW1116 cells. Then, we found that the protein ITGA5 was identified as a binding partner of FN1 and ITGA5 overexpression reversed FN1‐induced tumorigenesis of CRC in vitro. Taken together, FN1 suppressed apoptosis and promoted viability, invasion and migration in CRC through interacting with ITGA5. FN1 may be a prognostic factor and potential target for CRC treatment. This article is protected by copyright. All rights reserved

Autoren:   Xun Cai, Chuan Liu, Tie‐ning Zhang, Yi‐wen Zhu, Xiao Dong, Peng Xue
Journal:   Journal of Cellular Biochemistry
Jahrgang:   2017
Seiten:   n/a
DOI:   10.1002/jcb.26651
Erscheinungsdatum:   23.12.2017
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