Inhibition Mechanism Research about CD59 Specific Site Closed Short Peptide on T Cell Leukemia

Inhibition Mechanism Research about CD59 Specific Site Closed Short Peptide on T Cell Leukemia

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Author(s): GAO Meihua, Zhong WANG, Bing LI, Huaqiao LI, Beibei CONG, Yi WANG, Fengyu ZHANG, Le XIONG

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DOI: 10.18483/ijSci.1169 432 607 20-27 Volume 5 - Dec 2016


Objective: To study SP22 the closed short peptide of CD59 specific site on Jurkat cell signal transduction molecules (LAT, STAT3) genes, proliferation genes (Nf-κb3, Bcl-2) and apoptosis genes (caspase-3) effect, research CD59 specific site closed by short peptide concrete mechanism of Jurkat cells. Methods: Jurkat cells were divided into blank control group and SP22 peptide closed group, Training after 48h respectively with the method of CCK 8 to detect each cell proliferation rate; Flow cytometry -- check each group cell apoptosis; Real time quantitative PCR --from gene level determination of two kinds of cells before and after the experiment the expression of stat3 and joint protein Lat, detection of cell proliferation and apoptosis protein before and after test the Nf-κb3, Bcl-2, the expression of Caspas-3; Enzyme-linked immunosorbent assay (ELISA) to detect the related cytokines. Results: add SP22 peptide group cell proliferation inhibition rate is greater than the blank control group (P < 0.01);Add SP22 group compared with blank control group Lat, Stat3, Nf-κb3, Bcl-2 gene expression decline, Caspas-3 gene expression rise; Add SP22 40 mg group cell death ratio increased, compared with the blank control group difference has statistically significant (P < 0.01). In short peptide SP22 group, cells secrete and promote tumor to growth of interleukin 2 (IL-2) and TGF-βhad been inhibited. Conclusion: CD59 specific site closed short peptide can inhibit Jurkat cell proliferation, reduce the expression of Lat, Stat3, Nf-κb and Bcl-2, activating caspase-3, promote the apoptosis of Jurkat cells.


CD59, Close peptideSP22, Jurkat cell, Apoptosis


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