ArticleIntegrative cancer therapies
A Promising Natural Red Pigment "Prodigiosin" Sensitizes Colon Cancer Cells to Ionizing Radiation, Induces Apoptosis, and Impedes MAPK/TNF-α/NLRP3 Signaling Pathway.
Article in Integrative cancer therapies. 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.
- Prodigiosin Enhanced TMZ Chemosensitivity by Suppressing Focal Adhesion and Inhibiting Autophagy in Glioblastoma Cells.Biomolecules · 2026Article
- Molecular Docking of Phytochemicals Involved in Apoptotic Pathway and Their Interactions withPlants (Basel, Switzerland) · 2026Article
- Engineering of Extracellular Vesicles for Targeted Delivery of Prodigiosin.Biotech (Basel (Switzerland)) · 2026Article
- Anticancer and immune effect of the extracted brownOpen veterinary journal · 2026Article
- Prodigiosin in glioblastoma: mechanistic pharmacology and rationale for its development as a radiosensitiser.Frontiers in pharmacology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon cancer is one of the most prevalent cancers worldwide and the second leading cause of cancer-related deaths. The goal of the present study was to investigate the role of Prodigiosin (PG) in promoting programed cell death in irradiated Caco-2 colon cancer cells. We examined the extent to which PG disrupts the BCL-2/caspase-3 and PPAR-γ signaling pathways and affects apoptosis in these cancer cells. The inflammatory markers COX2, PGE2, NO, TNFα, and the inflammosome NLRP-3, MAPK in addition to prooxidant/antioxidant balance is also under investigation. Caco-2 cells were irradiated with gamma rays (6 Gy) either with or without PG and the results revealed that, PG established IC50 equivalent to 357.27 μgl/ml in Caco-2 cells. The flowcytometric analysis (Annexin V), BCL-2 and caspase-3 showed that PG induces apoptosis for Caco-2 cells. Furthermore, the PG + gamma irradiated (R) group of Caco-2 cells showed significant down regulation in proliferation and inflammatory cascade induction followed by changes in redox tone (expressed by increase in SOD and GSH activities and decrease in MDA concentration), resulted in reduction of tumor growth. It could be concluded that PG has an anti-proliferative action on Caco-2 cells because of its capability to enhance apoptosis in addition to its capability to enhance response of Caco-2 cells to gamma radiation. Based on our findings in the present study we were able to demonstrate that the oxidative status as well as inflammatory responses are grave for determining the longevity, life span and reactivity of Caco-2 colon cancer cells upon exposure to PG unaccompanied or accompanied by gamma radiation. Prodigiosin might represent a valuable key in contesting development of drug resistance of cancer cells and it could raise the radio-sensitivity of cells when PG delivered in combination with radiation exposures.
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.