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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

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    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
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TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway

Xinqiang Zhu1,2 , Xuetong Jiang2 , Qinglin Zhang3 , Hailong Huang2 , Xiaohong Shi4 , Daorong Hou5 , and Chungen Xing1

1Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 2Department of General Surgery, The Affiliated Suqian Hospital of Xuzhou Medical University, Suqian,3Department of Gastroenterology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, 4Department of Pathology, The Affiliated Suqian Hospital of Xuzhou Medical University, Suqian, and 5Key Laboratory of Model Animal Research, Nanjing Medical University, Nanjing, China

Correspondence to:Chungen Xing
ORCID https://orcid.org/0000-0001-7865-1258
E-mail Xingcg@suda.edu.cn

Xinqiang Zhu, Xuetong Jiang, and Qinglin Zhang contributed equally to this work as first authors.

Received: October 28, 2021; Revised: January 21, 2022; Accepted: February 10, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gut Liver

Published online June 10, 2022

Copyright © Gut and Liver.

Abstract

Background/Aims: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC).
Methods: We studied the biological function of TCN1 by performing gain-of-function and loss-of-function analyses in HCT116 cell lines; examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells; and determined potential molecular mechanisms using HCT116 and SW480 CRC lines and mouse xenotransplantation models. Tumor xenograft and colonization assays were performed to detect the tumorigenicity and metastatic foci of cells in vivo.
Results: TCN1 knockdown attenuated CRC cell proliferation and invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism analyses showed that TCN1 interacted with integrin subunit β4 (ITGB4) to positively regulate the expression of ITGB4. TCN1 knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A. Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/plectin complex, leading to cytoskeletal damage.
Conclusions: TCN1 might play an oncogenic role in CRC by regulating the ITGB4 signaling pathway.

Keywords: TCN1, Proliferation, Invasion, Colorectal neoplasms, ITGB4 pathway


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Gut and Liver

Published online June 10, 2022

Copyright © Gut and Liver.

TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway

Xinqiang Zhu1,2 , Xuetong Jiang2 , Qinglin Zhang3 , Hailong Huang2 , Xiaohong Shi4 , Daorong Hou5 , and Chungen Xing1

1Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, 2Department of General Surgery, The Affiliated Suqian Hospital of Xuzhou Medical University, Suqian,3Department of Gastroenterology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, 4Department of Pathology, The Affiliated Suqian Hospital of Xuzhou Medical University, Suqian, and 5Key Laboratory of Model Animal Research, Nanjing Medical University, Nanjing, China

Correspondence to:Chungen Xing
ORCID https://orcid.org/0000-0001-7865-1258
E-mail Xingcg@suda.edu.cn

Xinqiang Zhu, Xuetong Jiang, and Qinglin Zhang contributed equally to this work as first authors.

Received: October 28, 2021; Revised: January 21, 2022; Accepted: February 10, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background/Aims: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC).
Methods: We studied the biological function of TCN1 by performing gain-of-function and loss-of-function analyses in HCT116 cell lines; examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells; and determined potential molecular mechanisms using HCT116 and SW480 CRC lines and mouse xenotransplantation models. Tumor xenograft and colonization assays were performed to detect the tumorigenicity and metastatic foci of cells in vivo.
Results: TCN1 knockdown attenuated CRC cell proliferation and invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism analyses showed that TCN1 interacted with integrin subunit β4 (ITGB4) to positively regulate the expression of ITGB4. TCN1 knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A. Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/plectin complex, leading to cytoskeletal damage.
Conclusions: TCN1 might play an oncogenic role in CRC by regulating the ITGB4 signaling pathway.

Keywords: TCN1, Proliferation, Invasion, Colorectal neoplasms, ITGB4 pathway

Gut and Liver

Vol.16 No.3
May, 2022

pISSN 1976-2283
eISSN 2005-1212

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