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HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
Published on: July 20, 2016
Integrated gene co-expression network analysis and experimental validation revealed potential targets of human urine
Lei Jiang1, Haoyuan Hong2, Shulin Xiang1
1Department of Critical Care Medicine, Intensive Care Unit, The People's Hospital of Guangxi Zhuang Autonomous Region, No. 6 Taoyuan Road, Qingxiu District, Nanning 530021, China.
Background:
Cell differentiation agent II (CDA-II) exhibits potent anti-proliferative and apoptosis-inducing properties against a variety of cancer cells. However, its mechanism of action in chronic myeloid leukemia (CML) remains unclear.
Methods:
Cell counting Kit 8 (CCK-8) and flow cytometry were used to investigate the effects of CDA-II on the biological characteristics of K562 cells. Gene (mRNA and lncRNA) expression profiles were analyzed by bioinformatics to screen differentially expressed genes and to perform enrichment analysis. The Pearson correlation coefficients of lncRNAs and mRNAs were calculated using gene expression values, and a lncRNA/mRNA co-expression network was constructed. The MCODE and cytoHubba plugins were used to analyze the co-expression network.
Results:
The Results, derived from CCK-8 and flow cytometry, indicated that CDA-II exerts dual effects on K562 cells: it inhibits their proliferation and induces apoptosis. From bioinformatics analysis, we identified 316 mRNAs and 32 lncRNAs. These mRNAs were predominantly related to the meiotic cell cycle, DNA methylation, transporter complex and peptidase regulator activity, complement and coagulation cascades, protein digestion and absorption, and cell adhesion molecule signaling pathways. The co-expression network comprised of 163 lncRNA/mRNA interaction pairs. Notably, our analysis results implicated clustered histone gene families and five lncRNAs in the biological effects of CDA-II on K562 cells.
Conclusion:
This study highlights the hub gene and lncRNA/mRNA co-expression network as crucial elements in the context of CDA-II treatment of CML. This insight not only enriches our understanding of CDA-II's mechanism of action but also might provide valuable clues for subsequent experimental studies of CDA-II, and potentially contribute to the discovery of new therapeutic targets for CML.
Insights
Cell differentiation agent II (CDA-II) inhibits chronic myeloid leukemia (CML) cell proliferation and induces apoptosis. Bioinformatics analysis revealed key lncRNA-mRNA interactions and histone gene involvement in CDA-II
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Cell differentiation agent II (CDA-II) shows anti-cancer properties.
- The mechanism of CDA-II in chronic myeloid leukemia (CML) is not well understood.
Purpose of the Study:
- To investigate the effects of CDA-II on K562 cells.
- To elucidate the molecular mechanisms underlying CDA-II's action in CML.
Main Methods:
- Cell counting Kit 8 (CCK-8) and flow cytometry assessed cell proliferation and apoptosis.
- Bioinformatics analysis identified differentially expressed mRNAs and lncRNAs.
- A lncRNA/mRNA co-expression network was constructed and analyzed.
Main Results:
- CDA-II inhibited K562 cell proliferation and induced apoptosis.
- 316 mRNAs and 32 lncRNAs were identified, linked to cell cycle, DNA methylation, and signaling pathways.
- A co-expression network revealed 163 lncRNA/mRNA pairs, implicating histone gene families and five lncRNAs.
Conclusions:
- The study identified key lncRNA-mRNA interactions and hub genes in CDA-II's mechanism.
- Findings enhance understanding of CDA-II's action in CML.
- Results may guide future research and therapeutic target discovery for CML.
