Downregulated IGFBP7 facilitates liver metastasis by modulating epithelial‑mesenchymal transition in colon cancer.
TL;DR: It is suggested that IGFBP7 may prevent colon cancer metastasis by inhibiting EMT, and serves as a potential diagnostic marker and therapeutic target for patients with colon cancer.
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Abstract: Distant metastasis is a major cause of cancer‑associated mortality in patients with colon cancer. Insulin‑like growth factor binding protein 7 (IGFBP7) has been identified as a crucial inhibitor of human cancer. However, the role of IGFBP7 in the pathogenesis of metastatic colon cancer has not been investigated. In the present study, the expression of IGFBP7 in 81 pairs of colon cancer tissues and adjacent normal tissues were investigated using immunohistochemistry. Furthermore, 24 pairs of primary colon cancer and matched liver metastasis tissues were analyzed. LοVο cells with IGFBP7‑knockdown and HT‑29 cells with IGFBP7‑overexpression were employed. The expression levels of E‑cadherin, N‑cadherin and Vimentin were quantified and compared. Significant alterations in the expression of IGFBP7 between late stage (III + IV) colon cancer and adjacent normal colonic mucosa were observed. (P=0.031). The association between IGFBP7 and epithelial‑mesenchymal transition (EMT) markers were validated in primary colon cancer and matched liver metastasis tissues. The invasive front of liver metastatic colon tissues revealed reduced IGFBP7 expression. Additionally, knockdown of IGFBP7 in LοVο cells resulted in decreased E‑cadherin, and increased N‑cadherin and Vimentin expression compared with the control group. Overexpression of IGFBP7 in HT‑29 cells induced an upregulation of E‑cadherin; however, the N‑cadherin and Vimentin levels were decreased. In conclusion, the results of the present study suggested that IGFBP7 may prevent colon cancer metastasis by inhibiting EMT, and serves as a potential diagnostic marker and therapeutic target for patients with colon cancer.
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Insulin Growth Factor Binding Protein 7 (IGFBP7)-Related Cancer and IGFBP3 and IGFBP7 Crosstalk.
TL;DR: An objective of this review is to present a comprehensive overview of the relationship between IGFBP7 and cancer, as well as highlighting IGFBP3 crosstalk with IGFBP 7 reported in recent studies.
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Xianyanling Yi,Xiaonan Zheng,Huan Xu,Jin Li,Tianyi Zhang,Peng Ge,Dazhou Liao,Hong Li,Xiaoyan Lyu,Jianzhong Ai +9 more
TL;DR: Overall, IGFBP7 plays a critical role in the immunoregulation and TME of B LCA and may serve as a novel potential target for combination treatment with immunotherapy for BLCA.
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Crosstalk between Cancer Cells and Cancer-Associated Fibroblasts Mediated by TGF-β1–IGFBP7 Signaling Promotes the Progression of Infiltrative Gastric Cancer
Zhijun Hong,W. Xie,Huiqin Zhuo,Xujin Wei,Kang Wang,Jia-ping Cheng,Lingyun Lin,Jingjing Hou,Xin Chen,Jian Cai +9 more
TL;DR: It was demonstrated that XGC-1-derived TGF-β1 upregulated the expression of IGFBP7 in the cells and its secretion via the P-Smad2/3 pathway and mediated its activation with higher FAP, PDGFRB, and α-SMA expression.
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TL;DR: IGBP7 was found to be overexpressed in STAD, and its expression was closely associated with the clinical characteristics of STAD and showed promise as a biomarker for prediction and prognosis in pan-cancer.
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Angiogenesis modulated by CD93 and its natural ligands IGFBP7 and MMRN2: a new target to facilitate solid tumor therapy by vasculature normalization
Li Yang,Lei Fu,Baokang Wu,Xingqi Guo,Yu Shi,Chao Lv,Yanling Yu,Yizhou Zhang,Zhiyun Liang,Chongli Zhong,Sheng Han,Feng Xu,Yu Tian +12 more
TL;DR: Angiogenesis modulated by CD93 and its natural ligands IGFBP7 and MMRN2 is a new target to facilitate solid tumor therapy by vasculature normalization.
References
IGFBP7 plays a potential tumor suppressor role in colorectal carcinogenesis
Wenjing Ruan,Enping Xu,Fangying Xu,Yu Ma,Hong Deng,Qiong Huang,Bingjian Lv,Hu Hu,Jie Lin,Jing Cui,Meijuan Di,Jiankang Dong,Maode Lai +12 more
TL;DR: In this article, the authors investigated the function of IGFBP7 in colorectal adenocarcinoma (CRC) cell lines by transfection studies and found that the protein could inhibit cell growth, decrease soft agar colony formation activity and induce apoptosis in RKO and SW620 cells.
Revisiting epithelial-mesenchymal transition in cancer metastasis: the connection between epithelial plasticity and stemness
TL;DR: In summary, dynamic changes or plasticity between the epithelial and the mesenchymal states rather than a fixed phenotype is more likely to occur in tumors in the clinical setting.