Evidence map›Paper›PMID 41483432›Full record

ArticleDigestive diseases and sciences2026

Repression of Polycomb Group Factor 1 Inhibits EMT Progression in Colon Cancers Cells via Wnt/β-Catenin and PI3K/Akt/mTOR Signaling Pathway.

Peng An, Junhong Wang, Rong Fan

Abstract read
In one paragraph

Article in Digestive diseases and sciences, 2026. 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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0citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Peng An *Material Evidence Technology Center, School of Law, Tianjin University of Commerce, Tianjin, 300134, China. anpeng19831021@tjcu.edu.cn.
Junhong Wang *School of Medical Technology, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China.
Rong FanCentral Laboratory, Tianjin Xiqing Hospital, Tianjin, 300380, China. prosperity_39@sina.cn.

Funding

Health Commission of Hebei Province T2025025Tianjin Municipal Health Commission 2021031Tianjin Municipal Science and Technology Committee 21JCZDJC01070
6 · The paper itself

Abstract

backgroundThe study aimed to investigate polycomb group factor 1 (PCGF1) expression in colon cancer and its mechanism of action in the proliferation and migration of colon cancer cells.

methodIn this study, PCGF1 expression in colon cancer and the association between PCGF1 expression and the survival prognosis of patients with colon cancer were analyzed using the cancer genome atlas (TCGA) database. Furthermore, PCGF1 expression in normal colon epithelial cells and colon cancer cells was examined. A PCGF1 knockdown cell model was developed using HCT116 and HT29 cell lines. The effect of PCGF1 on cell proliferation was evaluated via CCK-8 and clone formation assays. In addition, the effect of PCGF1 on cell invasive and migratory abilities was explored via scratch and Transwell experiments, and the expression levels of EMT-related proteins was analyzed via immunoblotting assay.

resultsPCGF1 expression significantly increased in colon cancer tissues. This expression was also found to be closely associated with tumor staging of patients with colon cancer. High PCGF1 expression showed negative correlation with overall survival rate in these patients. The proliferative ability of HCT116 and HT29 cells knocked down by PCGF1 weakened, colony formation was reduced, and cell invasive and migratory capabilities diminished. Meanwhile, the expressions of EMT-related proteins, such as N-cadherin and Snail1, were remarkably downregulated in PCGF1 knockdown cells, whereas that of E-cadherin was significantly upregulated. Moreover, PCGF1 knockdown led to a strongly decrease in the phosphorylation levels of PI3K, Akt and mTOR proteins and in the levels of β-catenin and c-Myc.

conclusionPCGF1 may promote the proliferation and EMT process in HCT116 and HT29 cells by activating the Wnt/β-catenin and PI3K/Akt/mTOR signaling pathway.

Indexed as

Colonic NeoplasmsEpithelial-Mesenchymal TransitionPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesWnt Signaling Pathwaybeta CateninCell MovementCell ProliferationGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansPhosphatidylinositol 3-KinasesSignal Transductionbeta CateninCTNNB1 protein, humanMTOR protein, humanPhosphatidylinositol 3-KinasesPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAkt/mTOR signaling pathwayCOADEMTPCGF1Polycomb groupWnt/β-catenin signaling pathway

Identifiers

PMID41483432
PMCPMC13357582

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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 OpenQuestion graph.