ArticleMedical molecular morphology2015
SPARC is associated with carcinogenesis of oral squamous epithelium and consistent with cell competition.
Article in Medical molecular morphology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- miR-29a-3p regulates SPARC to inhibit ferroptosis and promote cell proliferation in gastric cancer.Scientific reports · 2026Article
- Detection of Merkel cell polyomavirus in multiple primary oral squamous cell carcinomas.Odontology · 2023Article
- Functions of Matricellular Proteins in Dental Tissues and Their Emerging Roles in Orofacial Tissue Development, Maintenance, and Disease.International journal of molecular sciences · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The matricellular protein, secreted protein acidic and rich in cysteine (SPARC) is thought to be involved in cell competition. The objective of this study is to investigate the role of SPARC in cancerization of oral squamous epithelium. Clinical specimens from 57 pre- and early cancerous lesion, 66 invasive squamous cell carcinoma (SCC) and controls were immunostained with SPARC. Clinical features and SPARC expression were evaluated. Furthermore, effects of SPARC knockdown and overexpression were examined in oral cancer and keratinocyte cell lines. Leukoplakia, carcinoma in situ, and early invasive SCC had more SPARC-positive cells than normal mucous epithelium. However, there were no significant differences between leukoplakia, carcinoma in situ, and early SCC, and there were no correlations between SPARC immunoreactivity and prognosis of invasive oral SCCs. Cell proliferation was down-regulated by SPARC siRNA, and enhanced by SPARC transformed keratinocytes. But SPARC overexpression did not enhance cell migration activity. SPARC is induced by dysplastic cells in the early stage of cancerization, and may improve survival capability, but is not involved in malignancy. SPARC may act to escape from elimination by cell competition.
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