ArticleCancer cell international2020
Skp2 modulates proliferation, senescence and tumorigenesis of glioma.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Oleic acid fuels cisplatin-resistant ovarian cancer through FABP4-driven lipid uptake.Molecular metabolism · 2026Article
- Total flavonoids of Litchi seed suppress liver cancer stem cell-like properties by inhibiting the SKP2/Shh signaling axis.Journal of pharmaceutical analysis · 2026Article
- Overcoming temozolomide resistance in glioma: recent advances and mechanistic insights.Acta neuropathologica communications · 2025Review
- Nicotinamide metabolism reprogramming drives reversible senescence of glioblastoma cells.Cellular and molecular life sciences : CMLS · 2025Article
- Raddeanin A (RA) Inhibited EMT and Stemness in Glioblastoma via downregulating Skp2.Journal of Cancer · 2025Article
- Targeting mitochondrial quality control: new therapeutic strategies for major diseases.Military Medical Research · 2024Review
- Identification of a miRNA multi-targeting therapeutic strategy in glioblastoma.Cell death & disease · 2023Article
- Cellular senescence in glioma.Journal of neuro-oncology · 2023Review
- A Review of the Regulatory Mechanisms of N-Myc on Cell Cycle.Molecules (Basel, Switzerland) · 2023Review
- Small-molecule compounds inhibiting S-phase kinase-associated protein 2: A review.Frontiers in pharmacology · 2023Review
- Driver mutations in ADGRL3 are involved in the evolution of ependymoma.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- SPDL1 Is an Independent Predictor of Patient Outcome in Colorectal Cancer.International journal of molecular sciences · 2022Article
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- Antitumoral Activities of Curcumin and Recent Advances to ImProve Its Oral Bioavailability.Biomedicines · 2021Review
- RIOK2 Inhibitor NSC139021 Exerts Anti-Tumor Effects on Glioblastoma via Inducing Skp2-Mediated Cell Cycle Arrest and Apoptosis.Biomedicines · 2021Article
- The multifaceted NF-kB: are there still prospects of its inhibition for clinical intervention in pediatric central nervous system tumors?Cellular and molecular life sciences : CMLS · 2021Review
- An Alternative Pipeline for Glioblastoma Therapeutics: A Systematic Review of Drug Repurposing in Glioblastoma.Cancers · 2021Review
- Hypoxia-Related lncRNA Correlates With Prognosis and Immune Microenvironment in Lower-Grade Glioma.Frontiers in immunology · 2021Article
- The Paradoxical Role of Cellular Senescence in Cancer.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGliomas represent the largest class of primary central nervous system neoplasms, many subtypes of which exhibit poor prognoses. Surgery followed by radiotherapy and chemotherapy has been used as a standard strategy but yielded unsatisfactory improvements in patient survival outcomes. The S-phase kinase protein 2 (Skp2), a critical component of the E3-ligase SCF complex, has been documented in tumorigenesis in various cancer types but its role in glioma has yet to be fully clarified. In this study, we investigated the function of Skp2 in the proliferation, stem cell maintenance, and drug sensitivity to temozolomide (TMZ) of glioma.
methodsTo investigate the role of Skp2 in the prognosis of patients with glioma, we first analyzed data in databases TCGA and GTEx. To further clarify the effect of Skp2 on glioma cell proliferation, we suppressed its level in glioblastoma (GBM) cell lines through knockdown and small molecule inhibitors (lovastatin and SZL-P1-41). We then detected cell growth, colony formation, sphere formation, drug sensitivity, and in vivo tumor formation in xenograft mice model.
resultsSkp2 mRNA level was higher in both low-grade glioma and GBM than normal brain tissues. The knockdown of Skp2 increased cell sensitivity to TMZ, decreased cell proliferation and tumorigenesis. In addition, Skp2 level was found increased upon stem cells enriching, while the knockdown of Skp2 led to reduced sphere numbers. Downregulation of Skp2 also induced senescence. Repurposing of lovastatin and novel compound SZL-P1-41 suppressed Skp2 effectively, and enhanced glioma cell sensitivity to TMZ in vitro and in vivo.
conclusionOur data demonstrated that Skp2 modulated glioma cell proliferation in vitro and in vivo, stem cell maintenance, and cell sensitivity to TMZ, which indicated that Skp2 could be a potential target for long-term treatment.
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