Evidence map›Paper›PMID 40729369›Full record

ArticlePLoS genetics2025

Identification of hub gene associated with colorectal cancer: Integrating Mendelian randomization, transcriptome analysis and experimental verification.

Yu Zhang, Xu Han, Yichun Yang, Jiayan Ren, Zixi Zhang, Yanmin Zhang, Qi Su, Dake Chu

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Article in PLoS genetics, 2025. 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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yu ZhangSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Xu HanSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Yichun YangSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Jiayan RenSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Zixi ZhangDepartment of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P. R. China.
Yanmin ZhangSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Qi SuSchool of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.ORCID https://orcid.org/0000-0002-7562-0429
Dake ChuDepartment of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P. R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is a prevalent malignancy with significant mortality rates globally. Understanding the genetic and molecular mechanisms underlying CRC development is crucial for improving therapeutic strategies.

methodIn this study, we utilized cis-eQTL summary data to identify genes potentially causally associated with CRC. The expression levels of candidate genes in tumor and normal tissues were compared using the GEPIA2 database. The correlations between FUT8 expression and cellular functions, tumor mutation burden, immune checkpoint genes, and immune infiltration were analyzed. Molecular docking was performed to identify potential drugs targeting FUT8, and the effects of the selected drug on cell proliferation were evaluated using the MTT assay. Additionally, the cellular thermal shift assay (CETSA) was employed to assess the interaction between the drug and the target protein.

resultsWe identified 19 genes with eQTLs potentially associated with CRC, among which six eQTLs were associated with increased CRC risk, including FUT8. FUT8 was significantly overexpressed in CRC tumor tissues and correlated with various cellular functions such as stemness, invasion, EMT, and metastasis. Higher FUT8 expression was associated with higher tumor mutation burden and significant correlations with multiple immune checkpoint genes. Molecular docking identified VE-822 as a promising drug candidate targeting FUT8, which demonstrated inhibitory effects on CRC cell proliferation. The CETSA results indicated that VE ‒ 822 could bind to FUT8 and improve its thermal stability.

conclusionFUT8 is a crucial gene that causes colon cancer and is linked to tumour immunity. VE-822 is a promising candidate for treating CRC by targeting FUT8.

Indexed as

Colorectal NeoplasmsFucosyltransferasesCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMendelian Randomization AnalysisMolecular Docking SimulationTranscriptomeFucosyltransferases

Identifiers

PMID40729369
PMCPMC12349882

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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.