Evidence map›Paper›PMID 42364020›Full record

ArticleMolecular biology reports2026

Filgotinib induces apoptosis in colorectal cancer cells by activating the p53 signaling pathway.

Ying Zhou, Zhen Li, Yanyang Zhao, Chenmeng Li, Huiming Ye

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Ying Zhou *School of Medicine, Xiamen University, No. 4221, Xiang'an South Road, Xiamen, 361102, China.
Zhen Li *School of Medicine, Xiamen University, No. 4221, Xiang'an South Road, Xiamen, 361102, China.
Yanyang ZhaoSchool of Public Health, Xiamen University, Xiamen, 361102, China.
Chenmeng LiDepartment of Laboratory Medicine, Fujian Key Clinical Specialty of Laboratory Medicine, Department of Gynecology and Obstetrics, Women and Children's Hospital, School of Medicine, Xiamen University, No. 10, Zhenhai Road, Xiamen, 361000, China. lichenmeng@xmu.edu.cn.
Huiming YeDepartment of Laboratory Medicine, Fujian Key Clinical Specialty of Laboratory Medicine, Department of Gynecology and Obstetrics, Women and Children's Hospital, School of Medicine, Xiamen University, No. 10, Zhenhai Road, Xiamen, 361000, China. yehuiming@xmu.edu.cn.

Funding

National Natural Science Foundation of China 82302898
6 · The paper itself

Abstract

backgroundColorectal cancer remains a significant health challenge. Filgotinib is a selective JAK1 inhibitor approved for the treatment of inflammatory diseases. However, its anti-tumor effects and underlying mechanisms in colorectal cancer (CRC) remain unexplored. METHODS AND

resultsIn this study, cell viability and proliferation were assessed by CCK‑8, crystal violet, and EdU assays. Mitochondrial membrane potential was evaluated using JC‑1 staining. Transcriptome sequencing (RNA‑seq) was performed on RKO cells treated with Filgotinib, followed by GO and KEGG pathway enrichment analyses. Protein expression was examined by Western blot. The effect of Filgotinib was further validated in three human CRC patient‑derived organoids (PDOs). Filgotinib at concentrations near the IC

conclusionsOur study demonstrates that Filgotinib exerts direct anti-tumor effects in CRC by triggering apoptosis, activating the p53 pathway, and inhibiting pro-survival VEGF and TNF pathways. These findings support its potential as a targeted therapeutic agent for CRC.

Indexed as

ApoptosisColorectal NeoplasmsPyridinesTriazolesTumor Suppressor Protein p53Cell Line, TumorCell ProliferationCell SurvivalGene Expression ProfilingGene Expression Regulation, NeoplasticHCT116 CellsHumansJanus Kinase 1Membrane Potential, MitochondrialSignal TransductionJAK1 protein, humanJanus Kinase 1PyridinesTP53 protein, humanTriazolesTumor Suppressor Protein p53ApoptosisColorectal cancerFilgotinibP53 signaling pathwayTranscriptome sequencing

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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.