Evidence map›Paper›PMID 40507922›Full record

ArticleInternational journal of molecular sciences2025

Glucosylceramide Synthase, a Key Enzyme in Sphingolipid Metabolism, Regulates Expression of Genes Accounting for Cancer Drug Resistance.

Md Saqline Mostaq, Lin Kang, Gauri A Patwardhan, Yunfeng Zhao, Runhua Shi, Yong-Yu Liu

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Central Roles of Glucosylceramide in Driving Cancer Pathogenesis.International journal of molecular sciences · 2025
    Review
  3. Article
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

6 authors.

Md Saqline MostaqSchool of Basic Pharmaceutical and Toxicological Sciences, University of Louisiana at Monroe, Monroe, LA 71201, USA.ORCID 0009-0002-2359-4481
Lin KangDepartment of Biomedical Affairs and Research, Edward Via College of Osteopathic Medicine, Monroe, LA 71203, USA.
Gauri A PatwardhanSchool of Basic Pharmaceutical and Toxicological Sciences, University of Louisiana at Monroe, Monroe, LA 71201, USA.
Yunfeng ZhaoDepartment of Pharmacology, Toxicology and Neuroscience, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA.ORCID 0000-0002-2122-2265
Runhua ShiDepartment of Internal Medicine, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA.
Yong-Yu LiuSchool of Basic Pharmaceutical and Toxicological Sciences, University of Louisiana at Monroe, Monroe, LA 71201, USA.ORCID 0000-0002-7968-0162

Funding

STABILITY' (symptomatic review during biologic therapy) Review in Inflammatory Bowel DiseaseP20GM103424 · NIGMS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI Konstantin G Kousoulas · 2012 to 2026
$57.4M
Ceramide glycosylation determines the stemness of cancer stem cellsR15CA167476 · NCI · UNIVERSITY OF LOUISIANA AT MONROE · PI LIU, YONG-YU · 2013 to 2013
$413k
Edward Via College of Osteopathic Medicine Delta-CRP 22, 23NCI NIH HHS R15 CA167476NCI NIH HHS R15CA167476NIGMS NIH HHS P20 GM103424NIGMS NIH HHS P20 GM103424-11
6 · The paper itself

Abstract

Emergent cancer drug resistance and further metastasis can mainly be attributed to altered expression levels and functional activities of multiple genes of cancer cells under chemotherapy. In response to challenge with anticancer drugs, enhanced ceramide glycosylation catalyzed by glucosylceramide synthase (GCS) confers drug resistance and enrichment with cancer stem cells. p53 mutations, which gain function in tumor progression, are prevalently extant in ovarian cancers. Via integrated gene expression assessments, we characterized GCS-responsive genes in ovarian cancer cells treated with dactinomycin. NCI/ADR-RES cells dominantly expressed a p53 mutant (7 aa deleted in exon-5) and displayed anti-apoptosis; however, silencing GCS expression rendered these cells sensitive to dactinomycin-induced apoptosis. Microarray analyses of NCI/ADR-RES and its GCS transfected sublines found that elevated GCS expression or ceramide glycosylation was associated with altered expression of 41 genes, notably coding for ABCB1, FGF2, ALDH1A3, apolipoprotein E, laminin 2, chemokine ligands, and IL6, with cellular resistance to induced apoptosis and enrichment with cancer stem cells, promoting cancer progression. These findings were further corroborated through integrated genomic analyses of ovarian cancer from The Cancer Genome Atlas (TCGA) and cancer resistance to platinum-based chemotherapy. Altogether, our present study indicates that altered ceramide glycosylation can modulate expression of these GCS-responsive genes and alter cancer cell attributes under chemotherapy.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticGlucosyltransferasesOvarian NeoplasmsSphingolipidsApoptosisCell Line, TumorFemaleGlycosylationHumansTumor Suppressor Protein p53ceramide glucosyltransferaseGlucosyltransferasesSphingolipidsTumor Suppressor Protein p53apoptosisdactinomycingene mutationglucosylceramide synthasemicroarrayovarian cancerp53 tumor suppressor

Identifiers

PMID40507922
PMCPMC12155275

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.