Evidence map›Paper›PMID 40182609›Full record

ArticleOncology letters2025

The feasible role of soluble E‑cadherin in spheroidogenesis of HCT116 colorectal cancer cells, a candidate biomarker for liquid biopsy.

In-Youb Chang, Hye-Jin Boo, Jin Won Hyun, Sang-Pil Yoon

Abstract read
In one paragraph

Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

In-Youb ChangDepartment of Anatomy, College of Medicine, Chosun University, Gwangju 61452, Republic of Korea.
Hye-Jin BooJeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Jin Won HyunJeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Sang-Pil YoonJeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although E-cadherin is known as a tumor suppressor via its effects on cell to cell adhesion, the effects of E-cadherin on malignant transformation have not yet been thoroughly investigated. In the present study, after malignant transformation was induced by spheroid formation in a fetal bovine serum-supplemented environment, the effects of soluble E-cadherin on the spheroidogenesis of colorectal cancer cells were investigated. E-cadherin knock-out (KO) was performed in HCT116 cells, targeting exon 3 of the CDH1 gene. A cell viability assay was performed to determine the proliferation and viability of wild type and CDH1 KO HCT116 cells after treatment with anticancer drugs. Spheroidogenesis was compared with or without exogenous E-cadherin, antibody against the ectodomain of E-cadherin (DECMA-1) and PD98059 treatment. In addition, morphometry, immunocytochemistry and western blotting were performed. Soluble E-cadherin in culture media was measured using an enzyme-linked immunosorbent assay. Firstly, CDH1 KO was confirmed by western blotting. Notably, the proliferation and viability of cells following treatment with 5-fluorouracil, epidermal growth factor receptor inhibitor and src kinase inhibitor were similar between the cell lines. Exogenous E-cadherin or DECMA-1 treatment did not affect spheroidogenesis, although long-term maintenance was slightly disturbed in CDH1 KO spheroids compared with that in wild type spheroids. In addition, E-cadherin was increased in spheroid culture as compared with that in conventional culture. Soluble E-cadherin was increased in a time-dependent manner, particularly in wild type HCT116 cells. PD98059 inhibited ERK activation and enhanced E-cadherin expression in conventional culture without affecting spheroidogenesis. These results suggested that soluble E-cadherin may be considered as a biomarker for colorectal cancer, although exogenous E-cadherin might not have a further role in malignant transformation.

Indexed as

biomarkercolorectal cancerliquid biopsymalignant transformationsoluble E-cadherin

Identifiers

PMID40182609
PMCPMC11967162

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