Fenling Zhou, Lu Chen, Zhen Liu, Yuli Cao, Cuilan Deng, Gexiu Liu, Chengcheng Liu
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Specific shRNA sequences were designed to target <i>CKS2</i> for the purpose of constructing a lentiviral expression vector, and therapeutic effects were assessed through analyses of cell proliferation, cell cycle distribution, and cell apoptosis.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>First, the study examined the increased transcriptional and protein levels of <i>CKS2</i> in BL and DLBCL through analysis of various databases and immunohistochemistry tests. Elevated <i>CKS2</i> expression was found to be correlated with a worse prognosis in BL and DLBCL patients, as evidenced by data from the TCGA and GEO databases. Enrichment analysis indicated that <i>CKS2</i> functions were primarily linked to protein kinase regulatory activity, G1/S phase transition of the cell cycle, and the p53 signaling pathway, among others. Second, stable suppression of <i>CKS2</i> gene expression in Raji and SUDHL6 cells using shRNA resulted in a significant inhibition of cell proliferation. Moreover, <i>CKS2</i>-shRNA induced G0/G1 cell cycle arrest and apoptosis by activating the p53 signaling pathway in Raji and SUDHL6 cells. Third, the combined treatment of <i>CKS2</i>-shRNA and etoposide exhibited a synergistic effect on the proliferation and apoptosis of Raji and SUDHL6 cells.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Our findings suggest that <i>CKS2</i> may play a critical role in the progression of BL and DLBCL and provide evidence for the potential therapeutic application of combining <i>CKS2</i>-shRNA and etoposide agents in the treatment of BL and DLBCL.</p>\n </section>\n </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"13 22","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.70435","citationCount":"0","resultStr":"{\"title\":\"Unveiling CKS2: A Key Player in Aggressive B-Cell Lymphoma Progression and a Target for Synergistic Therapy\",\"authors\":\"Fenling Zhou, Lu Chen, Zhen Liu, Yuli Cao, Cuilan Deng, Gexiu Liu, Chengcheng Liu\",\"doi\":\"10.1002/cam4.70435\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>The objective of this study was to investigate the expression levels and biological significance of <i>CKS2</i> in Burkitt cell lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL). 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Unveiling CKS2: A Key Player in Aggressive B-Cell Lymphoma Progression and a Target for Synergistic Therapy
Background
The objective of this study was to investigate the expression levels and biological significance of CKS2 in Burkitt cell lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL). Additionally, the potential synergistic anti-tumor effects of CKS2 knockdown in combination with etoposide in BL and DLBCL were explored for the first time.
Methods
Bioinformatics analysis was utilized to explore the transcriptional levels, prognostic value, and gene function enrichment of CKS2 in BL and DLBCL. Specific shRNA sequences were designed to target CKS2 for the purpose of constructing a lentiviral expression vector, and therapeutic effects were assessed through analyses of cell proliferation, cell cycle distribution, and cell apoptosis.
Results
First, the study examined the increased transcriptional and protein levels of CKS2 in BL and DLBCL through analysis of various databases and immunohistochemistry tests. Elevated CKS2 expression was found to be correlated with a worse prognosis in BL and DLBCL patients, as evidenced by data from the TCGA and GEO databases. Enrichment analysis indicated that CKS2 functions were primarily linked to protein kinase regulatory activity, G1/S phase transition of the cell cycle, and the p53 signaling pathway, among others. Second, stable suppression of CKS2 gene expression in Raji and SUDHL6 cells using shRNA resulted in a significant inhibition of cell proliferation. Moreover, CKS2-shRNA induced G0/G1 cell cycle arrest and apoptosis by activating the p53 signaling pathway in Raji and SUDHL6 cells. Third, the combined treatment of CKS2-shRNA and etoposide exhibited a synergistic effect on the proliferation and apoptosis of Raji and SUDHL6 cells.
Conclusions
Our findings suggest that CKS2 may play a critical role in the progression of BL and DLBCL and provide evidence for the potential therapeutic application of combining CKS2-shRNA and etoposide agents in the treatment of BL and DLBCL.
期刊介绍：
Cancer Medicine is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research from global biomedical researchers across the cancer sciences. The journal will consider submissions from all oncologic specialties, including, but not limited to, the following areas:
Clinical Cancer Research
Translational research ∙ clinical trials ∙ chemotherapy ∙ radiation therapy ∙ surgical therapy ∙ clinical observations ∙ clinical guidelines ∙ genetic consultation ∙ ethical considerations
Cancer Biology:
Molecular biology ∙ cellular biology ∙ molecular genetics ∙ genomics ∙ immunology ∙ epigenetics ∙ metabolic studies ∙ proteomics ∙ cytopathology ∙ carcinogenesis ∙ drug discovery and delivery.
Cancer Prevention:
Behavioral science ∙ psychosocial studies ∙ screening ∙ nutrition ∙ epidemiology and prevention ∙ community outreach.
Bioinformatics:
Gene expressions profiles ∙ gene regulation networks ∙ genome bioinformatics ∙ pathwayanalysis ∙ prognostic biomarkers.
Cancer Medicine publishes original research articles, systematic reviews, meta-analyses, and research methods papers, along with invited editorials and commentaries. Original research papers must report well-conducted research with conclusions supported by the data presented in the paper.
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