Evidence mapPaperPMID 39465374Full record

ArticleGenes & nutrition2024

Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways.

Chun-Te Lu, Jiunn-Liang Ko, Chu-Chyn Ou, Chih-Ting Hsu, Yu-Ping Hsiao, Sheau-Chung Tang

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Article in Genes & nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Chun-Te LuDivision of Plastic and Reconstructive Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, 407, Taiwan.
Jiunn-Liang KoInstitute of Medicine, School of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan.
Chu-Chyn OuDepartment of Nutrition, Chung Shan Medical University, Taichung, 402, Taiwan.
Chih-Ting HsuInstitute of Medicine, School of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan.
Yu-Ping HsiaoInstitute of Medicine, School of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan.
Sheau-Chung TangDepartment of Nursing, National Taichung University of Science and Technology, Taichung, 406, Taiwan. s6160051@nutc.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to evaluate soy isoflavones' effect and potential use-specifically genistein-in treating human keloid fibroblast cells (KFs) and in a keloid tissue culture model.

methodsTo investigate the effects of genistein on keloid, a wound-healing assay was performed to detect cell migration. Flow cytometry was used to measure apoptosis. Western blotting and immunofluorescence staining were performed to detect the expression of target proteins. KF tissues were isolated, cultured, and divided into the control, silenced connective tissue growth factor (CTGF) proteins, and shNC (negative control) groups.

resultsGenistein suppressed cell proliferation and migration, triggering the cell cycle at the G2/M phase and increasing the expression of p53 dose-dependent in keloids. Genistein inhibited the expression of COL1A1, FN, and CTGF mRNA and protein. Knockdown CTGF reduced the migrated ability in KFs. Genistein also abated TGF-β1-induced keloid fibrosis through the endocytosis model. Separated and cultured the keloid patient's tissues decreased the cell migration ability by genistein treatment and was time-dose dependent.

conclusionsThis study indicated that genistein-induced p53 undergoes cell cycle arrest via the CTGF pathway-inhibited keloid cultured cells, and genistein suppressed the primary keloid cell migration, suggesting that our research provides a new strategy for developing drugs for treating keloids.

Indexed as

CollagenCTGFFibronectinGenisteinKeloid

Identifiers

PMID39465374
PMCPMC11520065

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.