Evidence map›Paper›PMID 41771577›Full record

ArticleCancer genomics & proteomics

γ-Glutamylcyclotransferase Depletion Induces p15

Shigehisa Kubota, Hiromi Ii, Takahiro Isono, Takuto Kusaba, Masayuki Nagasawa, Akinori Wada, Kenichi Kobayashi, Kazuaki Yamanaka, Masaya Mori, Keiko Taniguchi and 2 more

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Article in Cancer genomics & proteomics. 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

What it found

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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

12 authors.

Shigehisa KubotaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Hiromi IiLaboratory of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Takahiro IsonoDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Takuto KusabaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Masayuki NagasawaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Akinori WadaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Kenichi KobayashiDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Kazuaki YamanakaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan.
Masaya MoriLaboratory of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Keiko TaniguchiDepartment of Drug Discovery Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Susumu NakataLaboratory of Clinical Oncology, Kyoto Pharmaceutical University, Kyoto, Japan.
Susumu KageyamaDepartment of Urology, Shiga University of Medical Science, Otsu, Japan; kageyama@belle.shiga-med.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimγ-Glutamylcyclotransferase (GGCT) depletion suppresses breast cancer cell proliferation by inducing cellular senescence. However, the underlying molecular mechanisms have not been fully elucidated. Therefore, the objective of this study was to elucidate the mechanisms by which GGCT depletion suppresses cancer cell proliferation. MATERIALS AND

methodsHuman breast cancer MCF-7 cells were transfected with GGCT-specific or control siRNAs. Transcriptomic profiling by RNA sequencing identified differentially expressed genes (

resultsComprehensive gene expression analysis revealed that depletion of

conclusionActivation of the TGF-β2/SMAD3 pathway is a mechanism by which cellular senescence is induced through GGCT depletion, suggesting that GGCT inhibition represents a promising therapeutic strategy for the treatment of breast cancer.

Indexed as

Breast NeoplasmsCellular SenescenceCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21gamma-GlutamylcyclotransferaseSmad3 ProteinTransforming Growth Factor beta2Cell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsSignal TransductionCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21gamma-GlutamylcyclotransferaseGGCT protein, humanSmad3 ProteinSMAD3 protein, humanTGFB2 protein, humanTransforming Growth Factor beta2cellular senescencecyclin-dependent kinase inhibitorGGCTSMADTGF-βtranscriptome analysisγ-Glutamylcyclotransferase

Identifiers

PMID41771577
PMCPMC12951391

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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.