ArticleInternational journal of molecular sciences2016
Survivin Modulates Squamous Cell Carcinoma-Derived Stem-Like Cell Proliferation, Viability and Tumor Formation in Vivo.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Identified BIRC5 and HDAC1 as novel diagnostic biomarkers linked to centrosome-immune crosstalk for cutaneous squamous cell carcinoma via machine learning-based multi-omics analysis.Discover oncology · 2026Article
- Exploring the Complexity of Cutaneous Squamous CellCarcinoma Microenvironment: Focus on Immune Cell Roles by Novel 3D In Vitro Models.Life (Basel, Switzerland) · 2025Review
- Investigating Cutaneous Squamous Cell CarcinomaFrontiers in medicine · 2022Review
- Do DLX3 and CD271 Protect Human Keratinocytes from Squamous Tumor Development?International journal of molecular sciences · 2019Article
- Targeted Therapy Against the Cell of Origin in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
- HOXA9 inhibits HIF-1α-mediated glycolysis through interacting with CRIP2 to repress cutaneous squamous cell carcinoma development.Nature communications · 2018Article
- p63 is a key regulator of iRHOM2 signalling in the keratinocyte stress response.Nature communications · 2018Article
- Transcriptional suppression of microRNA-27a contributes to laryngeal cancer differentiation via GSK-3β-involved Wnt/β-catenin pathway.Oncotarget · 2017Article
- Survivin, a molecular target for therapeutic interventions in squamous cell carcinoma.Cellular & molecular biology letters · 2017Review
- Stem Cell Activation in Adult Organisms.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Squamous Cell Carcinoma-derived Stem-like Cells (SCC-SC) originate from alterations in keratinocyte stem cells (KSC) gene expression and sustain tumor development, invasion and recurrence. Since survivin, a KSC marker, is highly expressed in SCC-SC, we evaluate its role in SCC-SC cell growth and SCC models. Survivin silencing by siRNA decreases clonal growth of SCC keratinocytes and viability of total, rapidly adhering (RAD) and non-RAD (NRAD) cells from primary SCC. Similarly, survivin silencing reduces the expression of stem cell markers (OCT4, NOTCH1, CD133, β₁-integrin), while it increases the level of differentiation markers (K10, involucrin). Moreover, survivin silencing improves the malignant phenotype of SCC 3D-reconstruct, as demonstrated by reduced epidermal thickness, lower Ki-67 positive cell number, and decreased expression of MMP9 and psoriasin. Furthermore, survivin depletion by siRNA in Ras(G12V)-IκBα-derived tumors leads to smaller tumor formation characterized by lower mitotic index and reduced expression of the tumor-associated marker HIF1α, VEGF and CD51. Therefore, our results indicate survivin as a key gene in regulating SCC cancer stem cell formation and cSCC development.
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Registered trials
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