ArticleVirologica Sinica2021
SOX5 Regulates Cell Proliferation, Apoptosis, Migration and Invasion in KSHV-Infected Cells.
Article in Virologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Pan-cancer analysis of the oncogenic role of SRY-related high-mobility group box protein B5 in human tumors.Experimental and therapeutic medicine · 2026Article
- CCL28 contributes to angiogenesis and cardiac repair through CCR10Nature communications · 2025Article
- A missense variant in the SOX5 gene (c.221C > T) is associated with intellectual disability.Orphanet journal of rare diseases · 2025Article
- Clinical Significance of SOX10 Expression in Human Pathology.Current issues in molecular biology · 2023Review
- Article
- Nanog, Stat-3, and Sox-5 involvement in human fetal temporomandibular joint late development.Journal of oral biology and craniofacial researchArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma (KS) originates from vascular endothelial cells, with KS-associated herpesvirus (KSHV) as the etiological agent. SRY-box transcription factor 5 (SOX5) plays different roles in various types of cancer, although its role in KS remains poorly understood. In this study, we identified the role of SOX5 in KS tissues and KSHV-infected cells and elucidated the molecular mechanism. Thirty-two KS patients were enrolled in this study. Measurement of SOX5 mRNA and protein levels in human KS tissues and adjacent control tissues revealed lower levels in KS tissues, with KS patients having higher SOX5 level in the early stages of the disease compared to the later stages. And SOX5 mRNA and protein was also lower in KSHV-infected cells (iSLK-219 and iSLK-BAC) than normal cells (iSLK-Puro). Additionally, SOX5 overexpression inhibited cell proliferation and promoted apoptosis and decreased KSHV-infected cell migration and invasion. Moreover, we found that SOX5 overexpression suppressed the epithelial-to-mesenchymal transition of KSHV-infected cells. These results suggest SOX5 is a suppressor factor during KS development and a potential target for KS treatment.
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