临床与实验病理学杂志
臨床與實驗病理學雜誌
림상여실험병이학잡지
Chinese Journal of Clinical and Experimental Pathology
2015年
8期
890-894
,共5页
苏曙光%王晓华%赵震%郭经锋
囌曙光%王曉華%趙震%郭經鋒
소서광%왕효화%조진%곽경봉
肝肿瘤%RNase MC2%细胞周期%细胞自噬
肝腫瘤%RNase MC2%細胞週期%細胞自噬
간종류%RNase MC2%세포주기%세포자서
liver neoplasms%RNase MC2%cell cycle%autophagy
目的:探讨苦瓜子有效成分RNA酶MC2(RNase MC2)在肝癌细胞生长中的作用及其机制。方法应用MTT、克隆形成和体内裸鼠成瘤实验研究RNase MC2对肝癌细胞增殖的影响,流式细胞技术检测RNase MC2对肝癌细胞周期的影响,电镜检测RNase MC2诱导的细胞自噬,Western blot法检测RNase MC2作用引起的蛋白变化。结果体内外实验结果显示RNase MC2显著抑制肝癌细胞增殖;上调p53和p21蛋白表达导致G2/M期阻滞;增加Beclin-1和LC3-Ⅱ蛋白表达诱导细胞自噬。RNase MC2在体内外均能增强Sorafenib对肝癌细胞的杀伤能力。结论苦瓜子有效成分RNase MC2可能通过细胞周期阻滞、诱导细胞自噬而显著抑制肝癌细胞的生长,并可增强Sorafenib对肝癌细胞的治疗效果。
目的:探討苦瓜子有效成分RNA酶MC2(RNase MC2)在肝癌細胞生長中的作用及其機製。方法應用MTT、剋隆形成和體內裸鼠成瘤實驗研究RNase MC2對肝癌細胞增殖的影響,流式細胞技術檢測RNase MC2對肝癌細胞週期的影響,電鏡檢測RNase MC2誘導的細胞自噬,Western blot法檢測RNase MC2作用引起的蛋白變化。結果體內外實驗結果顯示RNase MC2顯著抑製肝癌細胞增殖;上調p53和p21蛋白錶達導緻G2/M期阻滯;增加Beclin-1和LC3-Ⅱ蛋白錶達誘導細胞自噬。RNase MC2在體內外均能增彊Sorafenib對肝癌細胞的殺傷能力。結論苦瓜子有效成分RNase MC2可能通過細胞週期阻滯、誘導細胞自噬而顯著抑製肝癌細胞的生長,併可增彊Sorafenib對肝癌細胞的治療效果。
목적:탐토고과자유효성분RNA매MC2(RNase MC2)재간암세포생장중적작용급기궤제。방법응용MTT、극륭형성화체내라서성류실험연구RNase MC2대간암세포증식적영향,류식세포기술검측RNase MC2대간암세포주기적영향,전경검측RNase MC2유도적세포자서,Western blot법검측RNase MC2작용인기적단백변화。결과체내외실험결과현시RNase MC2현저억제간암세포증식;상조p53화p21단백표체도치G2/M기조체;증가Beclin-1화LC3-Ⅱ단백표체유도세포자서。RNase MC2재체내외균능증강Sorafenib대간암세포적살상능력。결론고과자유효성분RNase MC2가능통과세포주기조체、유도세포자서이현저억제간암세포적생장,병가증강Sorafenib대간암세포적치료효과。
Purpose To determine the effect of RNase MC2 purified from momordica charantia on cell growth of hepatocellular carcino-ma ( HCC) and its underlying mechanism. Methods MTT, colony formation and nude mice model were used to examine the activity of RNase MC2 in cell proliferation. Cell cycle analysis was done by flow cytometry. Autophagy induced by RNase MC2 treatment was observed via transmission electron microscope. Western blot was performed to detect the RNase MC2-mediated changes of proteins. Re-sults In vitro and in vivo data showed that RNase MC2 markedly inhibited HCC cell proliferation, arrested cells at G2/M phase by in-creasing expression of p53 and p21, induced autophagy via upregulating Beclin-1 and LC3-Ⅱ. Furthermore, combination of RNase MC2 and Sorafenib exerted enhanced lethal effect on HCC cells. Conclusion RNase MC2 manifests significant antitumor activities and enhances the killing effect of Sorafenib in HCC via inducing cell cycle arrest and autophagy.