ArticleCells2025
Curcumin Inhibits Protease Activated Receptor 2-Induced ERK Phosphorylation Calcium Mobilization and Anti-Apoptotic Signaling in Inflammation-Driven Colorectal Cancer Cells.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Review on the Mechanism of and Therapies Targeting PANoptosis in Ulcerative Colitis.Biomolecules · 2026Review
- Deciphering the cancer chemopreventive potential of phytochemicals: an integrative perspective on molecular targets and signaling networks.Cancer cell international · 2026Review
- Pharmacologic Modulation of the PAR-2-ERK Axis by Statins Converts Inflammatory Survival Signalling into Apoptosis in Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Advancing ulcerative colitis therapy: a review of 5-ASA synergy with traditional Chinese medicine and natural bioactive compounds.Frontiers in pharmacology · 2026Review
- Epigallocatechin Gallate as a Molecular Therapeutic in Heart Failure and Cardio-Oncology: Mechanistic Pathways and Translational Perspectives.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundChronic inflammation drives colorectal cancer (CRC) progression, with PAR-2, a G-protein coupled receptor, linking extracellular inflammatory signals to tumor-promoting pathways via ERK1/2 phosphorylation, calcium mobilization, TNF-α upregulation, and apoptosis suppression. While curcumin has notable anti-inflammatory and anti-cancer properties, its effects on PAR-2 signaling in inflammation-driven CRC remain underexplored.
objectiveThis study investigates how curcumin modulates PAR-2 expression and downstream oncogenic signaling in inflammation-driven CRC cells and explores its potential direct interaction with PAR-2 at the structural level.
methodsHT 29 and Caco-2 CRC cell lines were exposed to lipopolysaccharide (LPS) to induce an inflammatory phenotype, followed by treatment with curcumin at 50 µM and 100 µM. PAR-2 and PAR-1 expression, along with downstream markers including ERK1/2, p-ERK, TNF-α,
resultsCurcumin selectively downregulated PAR-2-but not PAR-1-at both transcript and protein levels in a dose-dependent manner. This downregulation was accompanied by suppression of ERK phosphorylation and calcium signaling, inhibition of TNF-α secretion, and reversal of the anti-apoptotic signaling axis (
conclusionsOur findings reveal that curcumin targets the PAR-2/ERK/TNF-α axis and reactivates apoptotic pathways in inflammation-driven CRC, establishing it as a potent, mechanistically validated candidate for therapeutic repurposing in CRC.
Indexed as
Identifiers
What Socratic holds
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.