Evidence map›Paper›PMID 41721713›Full record

ArticleFuture science OA2026

Targeting FMO3 suppresses the malignant phenotype of colorectal cancer: evidence from bioinformatics to functional experiments.

Rong Su, Cuncun Huang, Zhe Jing, Shuping Qiu, Lihua Shao, Tinghong Jiao, Hongwei Wang, Hailong Li

Abstract read
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
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

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.

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

8 authors.

Rong SuDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0002-3385-0899
Cuncun HuangDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0003-4497-0674
Zhe JingDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0001-3040-6322
Shuping QiuDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0001-4752-3277
Lihua ShaoDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0006-0263-5482
Tinghong JiaoDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.
Hongwei WangLaboratory of Clinical Examination, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou, P.R. China.ORCID 0009-0000-6518-9500
Hailong LiDepartment of Internal Medicine, First School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, P.R. China.ORCID 0000-0002-5972-907X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsFlavin-containing monooxygenase 3 (FMO3) is a key metabolic enzyme involved in endogenous metabolism; however, its role in colorectal cancer (CRC) remains poorly understood. This study aimed to investigate the expression pattern, biological function, and potential clinical relevance of FMO3 in CRC. MATERIALS AND

methodsPublicly available transcriptomic datasets were analyzed to assess FMO3 expression and its association with clinical characteristics. Immunohistochemistry and in vitro functional assays were performed to evaluate the effects of FMO3 on CRC cell proliferation, cell-cycle progression, migration, and invasion. Bioinformatics analyses were used to explore potential signaling pathways and immune-related associations.

resultsFMO3 was significantly upregulated in CRC tissues and cell lines and was associated with unfavorable clinicopathological features and poor prognosis. Silencing of FMO3 inhibited CRC cell proliferation by inducing G0/G1 cell-cycle arrest and suppressed migration and invasion by reversing epithelial-mesenchymal transition-related phenotypes. Mechanistically, FMO3 depletion attenuated PI3K/AKT signaling activity. In addition, FMO3 expression was correlated with immune cell infiltration patterns and immune checkpoint-related molecules.

conclusionsFMO3 promotes malignant progression of colorectal cancer and may serve as a potential biomarker and therapeutic target. Further in vivo and mechanistic studies are warranted to validate these findings.

Indexed as

bioinformatics analysiscolorectal cancerFMO3PI3K/AKT signalingTMAO

Identifiers

PMID41721713
PMCPMC12928650

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