ArticleMolecular cancer2014
SPARC mediates metastatic cooperation between CSC and non-CSC prostate cancer cell subpopulations.
Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- SPARC family proteins: matricellular modulators of cancer progression and therapeutic resistance.Cancer gene therapy · 2026Review
- Omics Investigations of Prostate Cancer Cells Exposed to Simulated Microgravity Conditions.Biomolecules · 2025Article
- Subpopulation commensalism promotes Rac1-dependent invasion of single cells via laminin-332.The Journal of cell biology · 2024Article
- Joint analysis of mutational and transcriptional landscapes in human cancer reveals key perturbations during cancer evolution.Genome biology · 2024Article
- Cancer-associated fibroblasts and prostate cancer stem cells: crosstalk mechanisms and implications for disease progression.Frontiers in cell and developmental biology · 2024Review
- Omics Overview of the SPARC Gene in Mesothelioma.Biomolecules · 2023Review
- The paradox of cooperation among selfish cancer cells.Evolutionary applications · 2023Review
- Synergistic inter-clonal cooperation involving crosstalk, co-option and co-dependency can enhance the invasiveness of genetically distant cancer clones.BMC ecology and evolution · 2023Article
- Effect of SPARC Suppression in Mice, Perfused Human Anterior Segments, and Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2022Article
- SPARC Induces E-Cadherin Repression and Enhances Cell Migration through Integrin αvβ3 and the Transcription Factor ZEB1 in Prostate Cancer Cells.International journal of molecular sciences · 2022Article
- Statistical tests for intra-tumour clonal co-occurrence and exclusivity.PLoS computational biology · 2021Article
- Genetic diversity through social heterosis can increase virulence in RNA viral infections and cancer progression.Royal Society open science · 2021Article
- Review
- Review
- Hypoxic colorectal cancer cells promote metastasis of normoxic cancer cells depending on IL-8/p65 signaling pathway.Cell death & disease · 2020Article
- Bottom up proteomics reveals novel differentiation proteins in neuroblastoma cells treated with 13-cis retinoic acid.Journal of proteomics · 2019Article
- Genetic heterogeneity within collective invasion packs drives leader and follower cell phenotypes.Journal of cell science · 2019Article
- Metastasis as a systemic disease: molecular insights and clinical implications.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Genomic evolution of cancer models: perils and opportunities.Nature reviews. Cancer · 2019Review
- The Role of the Extracellular Matrix in Cancer Stemness.Frontiers in cell and developmental biology · 2019Article
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21 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor cell subpopulations can either compete with each other for nutrients and physical space within the tumor niche, or co-operate for enhanced survival, or replicative or metastatic capacities. Recently, we have described co-operative interactions between two clonal subpopulations derived from the PC-3 prostate cancer cell line, in which the invasiveness of a cancer stem cell (CSC)-enriched subpopulation (PC-3M, or M) is enhanced by a non-CSC subpopulation (PC-3S, or S), resulting in their accelerated metastatic dissemination.
methodsM and S secretomes were compared by SILAC (Stable Isotope Labeling by Aminoacids in Cell Culture). Invasive potential in vitro of M cells was analyzed by Transwell-Matrigel assays. M cells were co-injected with S cells in the dorsal prostate of immunodeficient mice and monitored by bioluminescence for tumor growth and metastatic dissemination. SPARC levels were determined by immunohistochemistry and real-time RT-PCR in tumors and by ELISA in plasma from patients with metastatic or non-metastatic prostate cancer.
resultsComparative secretome analysis yielded 213 proteins differentially secreted between M and S cells. Of these, the protein most abundantly secreted in S relative to M cells was SPARC. Immunodepletion of SPARC inhibited the enhanced invasiveness of M induced by S conditioned medium. Knock down of SPARC in S cells abrogated the capacity of its conditioned medium to enhance the in vitro invasiveness of M cells and compromised their potential to boost the metastatic behavior of M cells in vivo. In most primary human prostate cancer samples, SPARC was expressed in the epithelial tumoral compartment of metastatic cases.
conclusionsThe matricellular protein SPARC, secreted by a prostate cancer clonal tumor cell subpopulation displaying non-CSC properties, is a critical mediator of paracrine effects exerted on a distinct tumor cell subpopulation enriched in CSC. This paracrine interaction results in an enhanced metastatic behavior of the CSC-enriched tumor subpopulation. SPARC is expressed in the neoplastic cells of primary prostate cancer samples from metastatic cases, and could thus constitute a tumor progression biomarker and a therapeutic target in advanced prostate cancer.
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