ArticleMolecular carcinogenesis2026
IL-24 Induces Cell Dormancy and Oxaliplatin Resistance in Colon Cancer Cells by Activating NF-κB Pathway.
Article in Molecular carcinogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Oxaliplatin-based chemotherapy is a principal treatment for colon cancer, but drug resistance hinders its efficacy. Cancer cell dormancy is reportedly a crucial driver of chemoresistance. IL-24 functions vitally in tumor chemoresistance, yet its role in colon cancer dormancy and oxaliplatin resistance remains unexplored.IL-24 expression was assessed in colon cancer tissues and cells via RT-qPCR, western blotting, or immunohistochemistry. The functions of IL-24 in colon cancer cell proliferation, apoptosis, dormancy, and oxaliplatin resistance were evaluated by CCK-8, flow cytometry, and western blotting. The downstream mechanism of IL-24 was predicted using RNA sequencing and bioinformatics analyses and verified in vitro. A tumor xenograft mouse model was built to further verify the role of IL-24 in colon cancer. IL-24 was overexpressed in oxaliplatin-resistant colon cancer tissues and cells. Furthermore, IL-24 treatment reversed the anti-proliferative and pro-apoptotic effects of oxaliplatin on colon cancer cells. Regarding cell dormancy, IL-24 treatment triggered G0/G1 cell cycle arrest and upregulated dormancy markers (CDKN1A, CDKN1B, TGFB2, and MSK1). Bioinformatics analyses revealed that IL-24 might function in colon cancer mainly through NF-κB pathway, and IL-24 activated the NF-κB axis in tumor cells. Importantly, treatment with NF-κB inhibitor reversed IL-24-induced colon cancer cell dormancy and oxaliplatin resistance. In vivo, IL-24 treatment abolished the anti-tumor effects of oxaliplatin, promoted cell dormancy, and activated NF-κB signaling in tumor tissues. IL-24 induces colon cancer cell dormancy and oxaliplatin resistance by activating NF-κB signaling. The IL-24/NF-κB axis may serve as a likely target to alleviate oxaliplatin resistance in colon cancer.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.