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      IGFBP7 remodels the tumor microenvironment of esophageal squamous cell carcinoma by activating the TGFβ1/SMAD signaling pathway

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          Abstract

          Esophageal squamous cell carcinoma (ESCC) is the most common type of esophageal cancer, and its development, growth, and invasiveness are regulated by the tumor microenvironment (TME). Insulin-like growth factor-binding protein-7 (IGFBP7), which is closely related to various tumors, transforming growth factor-β1 (TGFβ1), which is a key signal mediator in oncogenesis, α-smooth muscle actin (α-SMA), and collagen I are important components of the TME. IGFBP7 can upregulate the expression of TGFβ1 and activate the TGFβ1/SMAD signaling pathway, which leads to an increase in collagen I in hepatic stellate cells (HSCs). However, the contribution of IGFBP7 to TGFβ1 and the TME in the progression of ESCC remains unknown. In the present study, we investigated IGFBP7 expression and its effects on TGFβ1 and the TME in ESCC. A total of 45 patients were divided into three groups: early-tumor group (n=15), advanced-tumor group (n=15), and paracancer control group (n=15). The EC109 cell line was cultured and treated with AdIGFBP7 and LvshTGFβ1, and the expression levels of IGFBP7, TGFβ1, α-SMA, collagen I, and p-SMAD2/3 were determined by immunohistochemical staining and western blotting analysis. IGFBP7, TGFβ1, α-SMA, and collagen I were upregulated in the ESCC samples compared with the control samples (P<0.05), and the values peaked in the advanced-tumor group (P<0.05). Compared with the control group, the TGFβ1, α-SMA, p-SMAD2/3, and collagen I proteins were gradually increased from 24 to 72 h in the EC109 cells treated with AdIGFBP7 (P<0.05). Inhibition of TGFβ1 expression in the EC109 cells treated with AdIGFBP7 gradually reduced the expression of α-SMA, collagen I, and p-SMAD2/3 from 24 to 72 h (P<0.05). These findings suggest that increased IGFBP7 may accelerate the progression of ESCC by upregulating TGFβ1, α-SMA, and collagen I via activating the TGFβ1/SMAD signaling pathway, which could remodel the TME.

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          New insights into TGF-β/Smad signaling in tissue fibrosis

          Ying-Yong Zhao, He-He Hu, Dan-Qian Chen … (2018)
          Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. This review presents an overview of the molecular mechanisms of TGF-β/Smad signaling pathway in renal, hepatic, pulmonary and cardiac fibrosis, followed by an in-depth discussion of their molecular mechanisms of intervention effects both in vitro and in vivo. The role of TGF-β/Smad signaling pathway in tumor or cancer is also discussed. Additionally, the current advances also highlight targeting TGF-β/Smad signaling pathway for the prevention of tissue fibrosis. The review reveals comprehensive pathophysiological mechanisms of tissue fibrosis. Particular challenges are presented and placed within the context of future applications against tissue fibrosis.
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            Esophageal carcinoma: Towards targeted therapies

            Ali Fatehi Hassanabad, Rania Chehade, Daniel Breadner … (2020)
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              ANRIL inhibits p15(INK4b) through the TGFβ1 signaling pathway in human esophageal squamous cell carcinoma.

              Deyu Chen, Zhaoyue Zhang, Chaoming Mao … (2014)
              The INK4b-ARF-INK4a gene cluster encodes three tumor suppressors: p15(INK4b), p14(ARF), and p16(INK4a). Antisense non-coding RNA in the INK4 locus (ANRIL) is transcribed in the opposite direction from this gene cluster. Recent studies suggest that ANRIL represses the expression of p15(INK4b), p14(ARF), and p16(INK4a); however, the underlying mechanism is unclear. In this study, the expressions of ANRIL in human esophageal squamous cell carcinoma (ESCC) tissues and matched adjacent non-tumor tissues were examined by quantitative real-time polymerase chain reaction. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor β1 (TGFβ1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFβ1 signaling pathways.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Lett
                Journal ID (iso-abbrev): Oncol Lett
                Journal ID (publisher-id): OL
                Title: Oncology Letters
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-1074
                ISSN (Electronic): 1792-1082
                Publication date Collection: August 2022
                Publication date (Electronic): 10 June 2022
                Publication date PMC-release: 10 June 2022
                Volume: 24
                Issue: 2
                Electronic Location Identifier: 251
                Affiliations
                [1 ]Department of Gastroenterology and Hepatology, Suzhou Xiangcheng People's Hospital, Suzhou, Jiangsu 215100, P.R. China
                [2 ]Department of Gastroenterology and Hepatology, Yangzhou University Medical College, Yangzhou, Jiangsu 225001, P.R. China
                [3 ]Department of Gastroenterology and Hepatology, Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University, Lianyungang, Jiangsu 222042, P.R. China
                [4 ]Department of Gastrointestinal and Anus Surgery, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Nanning, Guangxi 530012, P.R. China
                Author notes
                Correspondence to: Dr Liangliang Cai, Department of Gastrointestinal and Anus Surgery, The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, 89-9 Dongge Road, Nanning, Guangxi 530012, P.R. China, E-mail: okokokwcwcwc@ 123456163.com
                Article
                Publisher ID: OL-24-02-13371
                DOI: 10.3892/ol.2022.13371
                PMC ID: 9214703
                PubMed ID: 35761941
                SO-VID: e7138189-13d7-41c8-a35d-555d9aafd9b5
                Copyright © Copyright: © Li et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, 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.

                History
                Date received : 22 February 2022
                Date accepted : 25 May 2022
                Funding
                Funding: No funding was received.
                Categories
                Subject: Articles

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: esophageal squamous cell carcinoma,tumor microenvironment,insulin-like growth factor-binding protein-7,transforming growth factor-β1,α-smooth muscle actin,collagen i,p-smad2/3
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: esophageal squamous cell carcinoma, tumor microenvironment, insulin-like growth factor-binding protein-7, transforming growth factor-β1, α-smooth muscle actin, collagen i, p-smad2/3

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