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[目的]观察Biglycan及VEGF对结肠癌细胞系HCT116增殖、凋亡的影响并探讨其可能机制。[方法]向转染Biglycan的细胞系HCT116中转染VEGF siRNA,设对照组(Mock)、空载和干扰对照组(Vector+siRNA-NC)、Biglycan cDNA和干扰对照组(Biglycan+siRNA-NC)及Biglycan cDNA和VEGF干扰组(Biglycan+siRNA-VEGF)。Western Blot检测Biglycan、VEGF及Ki67、PCNA、P21的表达;MTT检测细胞增殖情况;流式细胞术检测细胞凋亡及周期。[结果]过表达Biglycan后,Ki67、PCNA和VEGF显著上调,P21显著下调。干扰VEGF后,上述3种周期蛋白的表达正好相反;Biglycan上调后,细胞增殖能力显著提高,下调VEGF后增殖能力又显著降低(P<0.05);Biglycan过表达后S期细胞总数(44.39%±1.80%)较Mock组(31.41%±1.81%)和Vector+siRNA-NC组(32.56%±1.07%)显著提高(P<0.01),凋亡率(0.12%±0.01%)较Mock组(1.75%±0.17%)和Vector+siRNA-NC组(1.83%±0.16%)显著下降(P<0.01);下调VEGF后S期细胞(20.76%±1.23%)显著降低(P<0.01),凋亡率(8.30%±0.71%)显著上升(P<0.01)。[结论]Biglycan通过促进VEGF的表达来促进结肠癌细胞的增殖并抑制其凋亡。
[Objective] To observe the effect of Biglycan and VEGF on the proliferation and apoptosis of colon cancer cell line HCT116 and to explore its possible mechanism. [Methods] VEGF siRNA was transfected into HCT116 cells transfected with Biglycan. Mock, Vector + siRNA-NC, Biglycan cDNA and Biglycan + siRNA-NC ) And Biglycan cDNA and VEGF interference group (Biglycan + siRNA-VEGF). The expression of Biglycan, VEGF, Ki67, PCNA and P21 were detected by Western Blot. The proliferation of cells was detected by MTT assay. The apoptosis and cell cycle were detected by flow cytometry. [Results] After over-expression of Biglycan, Ki67, PCNA and VEGF were significantly up-regulated and P21 was significantly down-regulated. After the expression of Biglycan was up-regulated, the cell proliferation ability was significantly increased, and the proliferation ability was significantly decreased after VEGF was down-regulated (P <0.05). The number of S phase cells after Biglycan overexpression was 44.39% ± 1.80%) was significantly higher than that in Mock group (31.41% ± 1.81%) and Vector + siRNA-NC group (32.56% ± 1.07%) (P <0.01) (P <0.01). The percentage of S phase cells (20.76% ± 1.23%) was significantly decreased (P <0.01) and apoptosis The rate (8.30% ± 0.71%) increased significantly (P <0.01). [Conclusion] Biglycan can promote the proliferation and inhibit the apoptosis of colon cancer cells by promoting the expression of VEGF.