ArticleScientific reports2017
Deficiency of CCN5/WISP-2-Driven Program in breast cancer Promotes Cancer Epithelial cells to mesenchymal stem cells and Breast Cancer growth.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Expression and clinical significance of CCN5 and the oestrogen receptor in advanced breast cancer.BMC women's health · 2025Article
- CCN5 Drives Leydig Cell Aging and Testicular Dysfunction: Insights into Fibrosis, Lipid Dysregulation, and Therapeutic Potential.Research (Washington, D.C.) · 2025Article
- Expressions and clinical significance of CCN5 and E-cadherin in primary and recurrent lesions of breast cancer.Frontiers in genetics · 2024Article
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- Nuclear respiratory factor-1 negatively regulates TGF-β1 and attenuates pulmonary fibrosis.iScience · 2022Article
- The TSP-1 domain of the matricellular protein CCN5 is essential for its nuclear localization and anti-fibrotic function.PloS one · 2022Article
- Matricellular Protein WISP2 Is an Endogenous Inhibitor of Collagen Linearization and Cancer Metastasis.Cancer research · 2021Article
- CCN5 activation by free or encapsulated EGCG is required to render triple-negative breast cancer cell viability and tumor progression.Pharmacology research & perspectives · 2021Article
- Clinical significance of CCN5 and mutant p53 in primary and recurrent lesions of breast cancer.American journal of translational research · 2021Article
- Monosomy 3 Influences Epithelial-Mesenchymal Transition Gene Expression in Uveal Melanoma Patients; Consequences for Liquid Biopsy.International journal of molecular sciences · 2020Article
- Downregulation of miR-506-3p Facilitates EGFR-TKI Resistance through Induction of Sonic Hedgehog Signaling in Non-Small-Cell Lung Cancer Cell Lines.International journal of molecular sciences · 2020Article
- Aspirin suppresses tumor cell-induced angiogenesis and their incongruity.Journal of cell communication and signaling · 2019Article
- Signaling Pathways Induced by Leptin during Epithelial⁻Mesenchymal Transition in Breast Cancer.International journal of molecular sciences · 2018Review
- CCN5 in alveolar epithelial proliferation and differentiation during neonatal lung oxygen injury.Journal of cell communication and signaling · 2018Article
- Racial disparity in breast cancer: can it be mattered for prognosis and therapy.Journal of cell communication and signaling · 2018Review
- Leptin-induced ER-α-positive breast cancer cell viability and migration is mediated by suppressing CCN5-signaling via activating JAK/AKT/STAT-pathway.BMC cancer · 2018Article
- RNA-seq Reveals the Overexpression of IGSF9 in Endometrial Cancer.Journal of oncology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer progression and relapse is conceivably due to tumor initiating cells (TICs)/cancer stem cells. EMT (epithelial-mesenchymal-transition)-signaling regulates TICs' turnover. However, the mechanisms associated with this episode are unclear. We show that, in triple-negative-breast cancer (TNBC) cells enriched with TICs, CCN5 significantly blocks cellular growth via apoptosis, reversing EMT-signaling and impairing mammosphere formation, thereby blocking the tumor-forming ability and invasive capacity of these cells. To corroborate these findings, we isolated tumor-initiating side populations (SP) and non-side population (NSP or main population) from MCF-7 cell line, and evaluated the impact of CCN5 on these subpopulations. CCN5 was overexpressed in the NSP but downregulated in the SP. Characteristically, NSP cells are ER-α positive and epithelial type with little tumorigenic potency, while SP cells are very similar to triple-negative ones that do not express ER-α- and Her-2 and are highly tumorigenic in xenograft models. The overexpression of CCN5 in SP results in EMT reversion, ER-α upregulation and delays in tumor growth in xenograft models. We reasoned that CCN5 distinguishes SP and NSP and could reprogram SP to NSP transition, thereby delaying tumor growth in the xenograft model. Collectively, we reveal how CCN5-signaling underlies the driving force to prevent TNBC growth and progression.
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Registered trials
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.