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目的:探讨野生型抑癌基因KLF6对前列腺癌LN-CaP细胞的生长增殖、细胞周期和侵袭转移能力的影响及其可能的作用机制.方法:利用RT-PCR法克隆目的基因KLF6,并将含KLF6的pEGFP-C1质粒转染入LNCaP细胞.分为转染组和对照组分别进行MTT法观察LNCaP细胞的生长抑制率,流式细胞仪观察细胞周期比例变化和凋亡率,细胞爬片划痕法观察LNCaP细胞的侵袭转移能力变化.结果:转染了野生型抑癌基因KLF6的前列腺癌LNCaP细胞生长抑制率为(31.9±4.7)%,对照组为0%,差异有统计学意义(P<0.01),细胞周期比例表现为G2/M期减少,G0/G1期比例增加为(75.0±8.8)%,对照组为(55.9±7.1)%,差异有统计学意义(P<0.05),细胞凋亡峰为(29.3±3.7)%,对照组为(8.6±0.9)%,差异有统计学意义(P<0.01);每毫米划痕区内迁移入的细胞数为102.8±15.4,对照组为(192.7±25.2),差异有统计学意义(P<0.05).结论:野生型抑癌基因KLF6的转染可以明显抑制前列腺癌LNCaP细胞的生长增殖,并诱导其调亡,使其侵袭转移能力下降,其机制可能与野生型抑癌基因KLF6部分地逆转LNCaP细胞的恶性表型有关.
Objective: To investigate the effect of wild-type anti-oncogene KLF6 on the proliferation, cell cycle, invasion and metastasis of prostate cancer LN-CaP cells and its possible mechanism.Methods: The target gene KLF6 was cloned by RT- KLF6 pEGFP-C1 plasmid transfected into LNCaP cells were divided into transfection group and control group respectively MTT assay LNCaP cell growth inhibition, flow cytometry to observe changes in cell cycle ratio and apoptosis rate, (LNCaP) transfected wild type tumor suppressor gene KLF6 was (31.9 ± 4.7)% in control group and 0% in control group, the difference was statistically significant ( (P <0.01). The proportion of cell cycle was decreased in G2 / M phase, the proportion of G0 / G1 phase was (75.0 ± 8.8)% and that of control group was (55.9 ± 7.1)%, , The apoptotic peak was (29.3 ± 3.7)% in the control group and (8.6 ± 0.9)% in the control group, with a significant difference (P <0.01); the number of migrating cells per millimeter of scratches was 102.8 ± 15.4, The control group was (192.7 ± 25.2), the difference was statistically significant (P0.05) .Conclusion: Transfection of wild type tumor suppressor gene KLF6 can be significantly inhibited LNCaP prostate cancer cell proliferation and induce apoptosis, it decreased invasion and metastasis, which may be partially reversed KLF6 the wild-type tumor suppressor gene malignant phenotype LNCaP cells.