ArticleMolecular biology of the cell2003
SPARC inhibits epithelial cell proliferation in part through stimulation of the transforming growth factor-beta-signaling system.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- Fighting Bleb Fibrosis After Glaucoma Surgery: Updated Focus on Key Players and Novel Targets for Therapy.International journal of molecular sciences · 2025Pooled it
- SPARC Drives Podocyte Mitochondrial Damage and Ferroptosis in Diabetic Kidney Disease Following Klotho Deficiency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protein-Based Nanomaterials for Cancer Therapy: A Comparative and Translational Perspective.Pharmaceutics · 2026Review
- Comparative proteomic analysis indicates differential responses to fumonisin BMycotoxin research · 2025Article
- Blood diagnostic biomarkers for neurologic manifestations of long COVID.Brain, behavior, & immunity - health · 2025Article
- Metabolic and Inflammatory Stimuli Impact Vascular Circulation and Cell Proliferation Processes in the Amygdala.Genes, brain, and behavior · 2025Article
- Hydrogel-Mediated Sustained Delivery of Corneal Epithelial Extracellular Vesicles: A Strategy for Enhanced Corneal Regeneration.ACS omega · 2025Article
- HDAC10 inhibition represses melanoma cell growth and BRAF inhibitor resistance via upregulating SPARC expression.NAR cancer · 2024Article
- SPARC Is Highly Expressed in Young Skin and Promotes Extracellular Matrix Integrity in Fibroblasts via the TGF-β Signaling Pathway.International journal of molecular sciences · 2023Article
- Identification of ORM1, vWF, SPARC, and PPBP as immune-related proteins involved in immune thrombocytopenia by quantitative LC-MS/MS.Clinical proteomics · 2023Article
- A role for GLUT3 in glioblastoma cell invasion that is not recapitulated by GLUT1.Cell adhesion & migration · 2021Article
- Bench to Bedside: Proteomic Biomarker Analysis of Cerebrospinal Fluid in Patients With Spondylomyelopathy.Cureus · 2021Review
- Combinatorial ECM Arrays Identify Cooperative Roles for Matricellular Proteins in Enhancing the Generation of TH+ Neurons From Human Pluripotent Cells.Frontiers in cell and developmental biology · 2021Article
- A phase II study of concurrent nab-paclitaxel/carboplatin combined with thoracic radiotherapy in locally advanced squamous cell lung cancer.Journal of thoracic disease · 2019Article
- Altered CSF Proteomic Profiling of Paediatric Acute Lymphocytic Leukemia Patients with CNS Infiltration.Journal of oncology · 2019Article
- Article
- TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology.International journal of molecular sciences · 2017Review
- The role of weekly nanoparticle albumin bound paclitaxel monotherapy as second line or later treatment for advanced NSCLC in China.Oncotarget · 2017Article
- Efficacy and safety of weekly intravenous nanoparticle albumin-bound paclitaxel for non-small cell lung cancer patients who have failed at least two prior systemic treatments.Thoracic cancer · 2017Article
- The SPARC protein: an overview of its role in lung cancer and pulmonary fibrosis and its potential role in chronic airways disease.British journal of pharmacology · 2017Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secreted protein, acidic and rich in cysteine (SPARC) is a multifunctional secreted protein that regulates cell-cell and cell-matrix interactions, leading to alterations in cell adhesion, motility, and proliferation. Although SPARC is expressed in epithelial cells, its ability to regulate epithelial cell growth remains largely unknown. We show herein that SPARC strongly inhibited DNA synthesis in transforming growth factor (TGF)-beta-sensitive Mv1Lu cells, whereas moderately inhibiting that in TGF-beta-insensitive Mv1Lu cells (i.e., R1B cells). Overexpression of dominant-negative Smad3 in Mv1Lu cells, which abrogated growth arrest by TGF-beta, also attenuated growth arrest stimulated by SPARC. Moreover, the extracellular calcium-binding domain of SPARC (i.e., SPARC-EC) was sufficient to inhibit Mv1Lu cell proliferation but not that of R1B cells. Similar to TGF-beta and thrombospondin-1, treatment of Mv1Lu cells with SPARC or SPARC-EC stimulated Smad2 phosphorylation and Smad2/3 nuclear translocation: the latter response to all agonists was abrogated in R1B cells or by pretreatment of Mv1Lu cells with neutralizing TGF-beta antibodies. SPARC also stimulated Smad2 phosphorylation in MB114 endothelial cells but had no effect on bone morphogenetic protein-regulated Smad1 phosphorylation in either Mv1Lu or MB114 cells. Finally, SPARC and SPARC-EC stimulated TGF-beta-responsive reporter gene expression through a TGF-beta receptor- and Smad2/3-dependent pathway in Mv1Lu cells. Collectively, our findings identify a novel mechanism whereby SPARC inhibits epithelial cell proliferation by selectively commandeering the TGF-beta signaling system, doing so through coupling of SPARC-EC to a TGF-beta receptor- and Smad2/3-dependent pathway.
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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.