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目的观察TAT-N24穿膜融合多肽抑制前列癌细胞增殖的作用。方法用纯化的TAT-N24穿膜融合多肽处理前列癌PC3细胞,采用流式细胞仪检测细胞周期进程的改变,BrdU掺入法检测其对细胞DNA合成的影响,Western blot法检测细胞内AKT蛋白的磷酸水平的变化。结果①细胞周期分布:空白组G0/G1期(56.9±6.1)%,S期(27.0±2.3)%,G2/M期(16.1±1.3)%;对照多肽组G0/G1期(57.9±4.8)%,S期(24.2±3.1)%,G2/M期(27.8±1.4)%;TAT-N24组G0/G1期(68.6±5.4)%(P<0.05),S期(19.4±1.5)%(P<0.05),G2/M期(12.3±1.4)%。②BrdU阳性细胞为空白组(37.9±3.2)%,对照多肽组(36.2±4.1)%,TAT-N24组(21.5±2.4)%(P<0.05);③AKT磷酸化水平组间差异无统计学意义。结论 TAT-N24穿膜融合多肽能有效阻滞前列腺癌PC3细胞的细胞周期进程,并抑制其DNA合成。TAT-N24穿膜融合多肽有望成为有效的治疗前列腺癌的分子靶向药物。
Objective To observe the effect of TAT-N24 transmembrane fusion polypeptide on the proliferation of prostate cancer cells. Methods PC3 cells were treated with purified TAT-N24 fusion peptide and the cell cycle progression was detected by flow cytometry. The effect of BrdU incorporation on the DNA synthesis was detected by Western blot. AKT protein Changes in the level of phosphoric acid. Results ① The cell cycle distribution: G0 / G1 phase (56.9 ± 6.1)%, S phase (27.0 ± 2.3)% and G2 / M phase (16.1 ± 1.3) ), S phase (24.2 ± 3.1)% and G2 / M phase (27.8 ± 1.4)% respectively in the TAT-N24 group and 68.6 ± 5.4% (P < % (P <0.05), G2 / M phase (12.3 ± 1.4)%. ②BrdU positive cells were blank group (37.9 ± 3.2)%, control polypeptide group (36.2 ± 4.1)% and TAT-N24 group (21.5 ± 2.4)% (P <0.05); ③ There was no significant difference in AKT phosphorylation between the two groups . Conclusion The TAT-N24 transmembrane fusion polypeptide can effectively block the cell cycle progression of PC3 cells and inhibit its DNA synthesis. TAT-N24 transmembrane fusion polypeptide is expected to be an effective molecular targeted drug for the treatment of prostate cancer.