Theaflavin-3,3′-Digallate Targets Pin1 to Suppress Hepatocellular Carcinoma Malignant Proliferation Through Modulation of MAPK and PI3K/AKT Signaling Pathways In Vitro

/M phase arrest. It also robustly inhibits HCC cell proliferation, invasion and migration, coinciding with downregulation of proteins governing cell cycle progression and invasive behavior. Transcriptome profiling coupled with enrichment analysis discovered that TF3 treatment differentially regulated 5009 genes, which were prominently enriched in pathways linked to apoptosis, cell cycle control, MAPK and PI3K/AKT signaling pathways. Western blotting analysis revealed that TF3 selectively suppresses phosphorylation of p38 and the PI3K/AKT cascade, activating JNK phosphorylation. In summary, our findings indicate that TF3 suppresses HCC proliferation by targeting Pin1, with attendant modulation of the MAPK and PI3K/AKT pathways, thereby presenting a potential candidate for targeted HCC therapy.

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Publication Details

Journal
Biomolecules
Published
2026-04-14
DOI
https://doi.org/10.3390/biom16040583
Primary Topic
Signaling Pathways in Disease
Type
article
Field-Weighted Citation Impact
0.00

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article

Theaflavin-3,3′-Digallate Targets Pin1 to Suppress Hepatocellular Carcinoma Malignant Proliferation Through Modulation of MAPK and PI3K/AKT Signaling Pathways In Vitro

Wenli Jiang, Shaoli lv, Ye Liu, Jiaxin Tao et al.
Biomolecules
Signaling Pathways in Disease
article

Theaflavin-3,3′-Digallate Targets Pin1 to Suppress Hepatocellular Carcinoma Malignant Proliferation Through Modulation of MAPK and PI3K/AKT Signaling Pathways In Vitro

Wenli Jiang, Shaoli lv, Ye Liu, Jiaxin Tao, Hui Zhong, Xiyuan Ouyang, Huaqing He, Jiayang Xie
article en

Abstract

/M phase arrest. It also robustly inhibits HCC cell proliferation, invasion and migration, coinciding with downregulation of proteins governing cell cycle progression and invasive behavior. Transcriptome profiling coupled with enrichment analysis discovered that TF3 treatment differentially regulated 5009 genes, which were prominently enriched in pathways linked to apoptosis, cell cycle control, MAPK and PI3K/AKT signaling pathways. Western blotting analysis revealed that TF3 selectively suppresses phosphorylation of p38 and the PI3K/AKT cascade, activating JNK phosphorylation. In summary, our findings indicate that TF3 suppresses HCC proliferation by targeting Pin1, with attendant modulation of the MAPK and PI3K/AKT pathways, thereby presenting a potential candidate for targeted HCC therapy.

BiomoleculesVol. 16(4)
Nanchang University (CN), Jiang Xi Institute for Drug Control (CN), Education Department of Jiangxi Province (CN)
National Natural Science Foundation of China, Education Department of Jiangxi Province, Jiangxi Provincial Department of Science and Technology
Openalex Percentile: Top 26%
Signaling Pathways in Disease
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