Breast-cancer-cell conditioned medium drove THP-1-derived macrophages toward a pro-inflammatory tumor-associated phenotype with higher IL-1beta, NLRP3, and caspase-1. Curcumin pretreatment reduced IL-1beta secretion, NLRP3 protein, and IL1B/CASP1 transcripts.
Key findings
- Conditioned medium increased IL-1beta and NLRP3/caspase-1 signals. Curcumin reduced IL-1beta secretion and NLRP3 protein and suppressed IL1B and CASP1 transcripts across multiple levels, although effect sizes, concentrations, and cytotoxicity are not given in the abstract.
Why this matters globally
Tumor-associated macrophages are relevant to inflammation and treatment resistance. This work adds a natural-product mechanism, but translation requires bioavailability, selectivity, broader immune effects, and combination-with-standard-therapy studies.
Thai researcher contribution
Chiang Mai University and Srinakharinwirot University collaborated with Korean researchers across bioengineering, pharmacology, and tumor inflammation.
Limitations to consider
This in vitro conditioned-medium model omits other immune cells, extracellular matrix, and pharmacokinetics. Pretreatment models prevention before exposure more than treatment after establishment, and cell viability and direct tumor-cell effects are not reported.
Verify the original sources
Journal of Cancer PreventionRead the original article↗DOI: 10.15430/jcp.26.026