SIRT1 Promotes Breast Cancer Stem Cell-Associated Properties and Represents a Potential Therapeutic Target.

Jianmin Ding, Baoxiang Guan, Xuejun Fan, Ningyan Zhang, Eva Sevick, Songlin Zhang

Abstract read

In one paragraph

Article in International journal of molecular sciences, 2026. 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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0citing papers 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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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Jianmin DingDepartment of Pathology & Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.ORCID 0009-0000-3916-1272

Baoxiang GuanDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.ORCID 0009-0004-7030-0292

Xuejun FanTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, 1825 Pressler Street, Houston, TX 77030, USA.

Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, 1825 Pressler Street, Houston, TX 77030, USA.ORCID 0000-0002-4348-2180

Eva SevickCenter of Molecular Imaging, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, 1825 Pressler Street, Houston, TX 77030, USA.ORCID 0000-0002-8152-4847

Songlin ZhangDepartment of Pathology & Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.ORCID 0009-0004-3811-2099

Funding

Baylor College of Medicine BC120177

6 · The paper itself

Abstract

Breast cancer stem cells (BCSCs) drive tumor progression, metastasis, and therapeutic resistance. Sirtuin 1 (SIRT1) has been implicated in stem cell regulation, but its context-dependent role in BCSC maintenance and the underlying molecular mechanisms remain poorly defined. SIRT1 expression was evaluated in human breast cancer specimens. Pharmacologic and genetic SIRT1 inhibition was assessed in breast cancer cell lines and orthotopic xenograft models to determine effects on stemness, epithelial-mesenchymal transition (EMT), metastasis, and chemoresistance, with emphasis on Wnt/β catenin signaling. SIRT1 was overexpressed in breast cancer and correlated with higher tumor grades. SIRT1 inhibition reduced BCSC markers (CD44, ALDH1), stemness genes (NANOG, SOX-2), mammosphere formation, EMT, and invasion. In vivo, SIRT1 inhibition suppressed tumor growth, blocked lymphatic metastasis, and delayed cisplatin resistance. Mechanistically, these effects were mediated by downregulation of Disheveled 3 (DVL3) and attenuation of Wnt/β catenin signaling. SIRT1 is associated with the maintenance of BCSC-related properties, EMT, and activation of the Wnt/β-catenin pathway in breast cancer. Targeting SIRT1 may represent a potential therapeutic strategy to suppress tumor progression and improve treatment response.

Indexed as

Breast NeoplasmsNeoplastic Stem CellsSirtuin 1AnimalsCell Line, TumorDishevelled ProteinsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMiceWnt Signaling PathwayDishevelled ProteinsSIRT1 protein, humanSirtuin 1breast cancerbreast cancer stem cell (BCSC)cancer stem cell (CSC)DVLepithelial–mesenchymal transition (EMT)SIRT1SIRT1 inhibitorTGF-βWnt/β-catenin pathway

Identifiers

PMID42794654

DOI10.3390/ijms27188226

PMCPMC13607794

What Socratic holds

Textmetadata

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.