Evidence map›Paper›PMID 40538846›Full record

ArticleFrontiers in oncology2025

GPD1L downregulation in colorectal cancer: a novel obesity-related biomarker linking metabolic dysregulation to tumor progression.

Feng Zhu, Huiyuan Li, Hongzhang Liu, Yusheng Wang

Abstract read
In one paragraph

Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Feng ZhuGeneral Surgery Department of Jincheng People's Hospital, Shanxi, China.
Huiyuan LiGeneral Surgery Department of Jincheng People's Hospital, Shanxi, China.
Hongzhang LiuGeneral Surgery Department of Jincheng People's Hospital, Shanxi, China.
Yusheng WangGeneral Surgery Department of Jincheng People's Hospital, Shanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To delineate the expression profile and tumor-suppressive function of the metabolism-associated gene GPD1L in colorectal carcinogenesis. Methods: Transcriptomic datasets from TCGA and GEO repositories (GSE74602, GSE113513, GSE164191) were computationally analyzed. Paired tumor/adjacent mucosal specimens (n=58) from CRC patients at Jincheng People's Hospital were analyzed alongside the NCM460 colon epithelial line and five CRC lines (SW620, HCT116, SW480, DLD-1, LOVO). Following GPD1L quantification via qPCR, selected cell models underwent pcDNA3.1-GPD1L transfection for functional characterization. Then Western blot analysis was used to explore its possible mechanism. Results: Comparative analysis revealed a marked elevation of GPD1L expression in non-neoplastic tissues relative to tumor specimens (P<0.001). Transcriptional profiling further identified significant depletion of GPD1L mRNA levels across malignant cell lines versus the NCM460 epithelial reference (P<0.05), with HCT116/SW620 showing maximal downregulation. Ectopic GPD1L expression attenuated oncogenic phenotypes: proliferation decreased (P<0.001), while Transwell quantification revealed 46.0% (HCT116: 605.0 ± 9.2 vs 326.7 ± 8.50 cells/field) and 54.3% (SW620: 455.3 ± 17.2 vs 208.0 ± 14.0 cells/field) reductions in migratory capacity (both P<0.001). Invasion assays showed parallel inhibition (HCT116: 43.3% decrease, P<0.01; SW620: 54.8% decrease, P<0.001). After overexpression of GPD1L, the expression levels of HIF-1α and MMP9 were reduced (P<0.05). Conclusion: GPD1L downregulation represents a hallmark of CRC progression, with affecting the expression of HIF-1α and MMP9 significantly impeding malignant behaviors, nominating it as a candidate tumor suppressor in colorectal neoplasia.

Indexed as

bioinformaticscolorectal cancerGPD1Lmetabolism-associated genetumor suppressor genes

Identifiers

PMID40538846
PMCPMC12177464

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