ArticleScientific reports2025
Targeting the p38/MAPK pathway to induce apoptosis: a multidimensional mechanistic exploration of Mentha and its active compound diosmetin against liver cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Identification of Changes in the Transcriptome Profile of Human Hepatoma HepG2 Cells Exposed to Combined Sorafenib and Cannabis Treatment.International journal of molecular sciences · 2026Article
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Liver cancer, a malignancy with high global incidence and mortality, currently relies on surgical resection, radiotherapy, and chemotherapy, all of which face significant limitations, necessitating novel therapeutic strategies. Mentha (ME), a medicinal and edible herb, has demonstrated antioxidant, anti-inflammatory, and broad-spectrum anticancer activities, yet its molecular mechanisms against liver cancer remain unclear. This study will comprehensively explore the anti-liver cancer mechanisms of ME and its key bioactive constituent, diosmetin (Dio). A multi-disciplinary approach, which incorporates network pharmacology, molecular docking, and molecular dynamics simulations, was adopted in this study to thoroughly explore the bioactive components of ME and the mechanisms through which they exert anti-liver cancer effects. Functional validation was conducted through CCK-8 viability assays, clonogenic survival assays, scratch wound healing, Transwell migration assays, Western blotting, immunofluorescence, and TUNEL apoptosis assays in human liver cancer cell lines (HepG2 and HuH-7). ME exhibited potent anti-Liver cancer activity, significantly suppressing cell viability, proliferation (CCK-8/clonogenic assays), and migration (scratch/Transwell assays, P < 0.01), while downregulating metastasis-related proteins MMP2/MMP9 (Western blot/immunofluorescence, P < 0.01). Network pharmacology identified TP53 (p53), TNF, CASP3 (caspase3), IL6, and IL1B as core targets. Based on the results of molecular docking (ΔG < - 4 kcal/mol) and molecular dynamics simulations (maximum ΔTotal), Dio was prioritized for subsequent experimental validation. Further validation demonstrated Dio's multi-modal efficacy: GO/KEGG analysis revealed its dual action via p38/MAPK signaling and apoptosis pathways, corroborated by upregulated pro-apoptotic markers (p53, caspase3, Bax, p38) and downregulated Bcl2 (P < 0.01), alongside TUNEL-confirmed apoptosis induction (P < 0.01). This study is the first to demonstrate that ME and its active compound Dio inhibit liver cancer progression via multi-target regulation of the p38/MAPK pathway, providing a theoretical foundation for developing ME-based natural therapeutics against liver cancer.
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Registered trials
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.