Evidence map›Paper›PMID 39560180›Full record

ArticleCancer medicine2024

Unveiling CKS2: A Key Player in Aggressive B-Cell Lymphoma Progression and a Target for Synergistic Therapy.

Fenling Zhou, Lu Chen, Zhen Liu, Yuli Cao, Cuilan Deng, Gexiu Liu, Chengcheng Liu

Abstract read
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Fenling ZhouDepartment of Hematology, Sun Yat-Sen Institute of Hematology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China.
Lu ChenInstitute of Hematology, Jinan University, Guangzhou, Guangdong, People's Republic of China.
Zhen LiuDepartment of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, People's Republic of China.
Yuli CaoInstitute of Hematology, Jinan University, Guangzhou, Guangdong, People's Republic of China.
Cuilan DengInstitute of Hematology, Jinan University, Guangzhou, Guangdong, People's Republic of China.
Gexiu LiuInstitute of Hematology, Jinan University, Guangzhou, Guangdong, People's Republic of China.
Chengcheng LiuDepartment of Hematology, Sun Yat-Sen Institute of Hematology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China.ORCID https://orcid.org/0000-0001-8693-9753

Funding

GuangZhou Basic and Applied Basic Research Foundation 202201010973GuangZhou Basic and Applied Basic Research Foundation 202201011474
6 · The paper itself

Abstract

backgroundThe 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.

methodsBioinformatics 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.

resultsFirst, 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.

conclusionsOur 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.

Indexed as

ApoptosisCDC2-CDC28 KinasesCell ProliferationEtoposideLymphoma, Large B-Cell, DiffuseBurkitt LymphomaCell CycleCell Cycle ProteinsCell Line, TumorComputational BiologyDisease ProgressionGene Expression Regulation, NeoplasticHumansPrognosisCDC2-CDC28 KinasesCell Cycle ProteinsCKS2 protein, humanEtoposidebioinformatics analysisBurkitt cell lymphoma (BL)cyclin‐dependent kinases regulatory subunit 2 (CKS2)diffuse large B‐cell lymphoma (DLBCL)etoposidetargeted therapy

Identifiers

PMID39560180
PMCPMC11574738

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