南方医科大学学报
南方醫科大學學報
남방의과대학학보
Journal of Southern Medical University
2015年
9期
1234-1238
,共5页
刘俊松%刘翔龙%仇广林%张正良%樊林%赵伟%贺仕才%常帅%车向明
劉俊鬆%劉翔龍%仇廣林%張正良%樊林%趙偉%賀仕纔%常帥%車嚮明
류준송%류상룡%구엄림%장정량%번림%조위%하사재%상수%차향명
β-榄香烯%胃癌%增殖%凋亡%Pak1%ERK
β-欖香烯%胃癌%增殖%凋亡%Pak1%ERK
β-람향희%위암%증식%조망%Pak1%ERK
β-Elemene%gastric cancer%proliferation%apoptosis%p21-activated protein kinase 1%extracellular signal-regulated kinases
目的:探讨β-榄香烯对胃癌细胞增殖和凋亡的影响及其可能的分子机制。方法通过四甲基偶氮唑盐比色法(MTT)、流式细胞术检测细胞凋亡、周期分布和平板克隆形成实验检测β-榄香烯对SGC7901胃癌细胞的影响,同时评价β-榄香烯对正常胃黏膜上皮细胞GES-1的毒性作用;通过Western blots检测β-榄香烯对SGC7901胃癌细胞的蛋白表达影响。结果β-榄香烯显著抑制SGC7901胃癌细胞的活性并诱导细胞凋亡,两种作用在正常胃黏膜上皮细胞GES-1中明显减弱。β-榄香烯降低SGC7901胃癌细胞克隆形成率,诱导SGC7901细胞发生G2/M期阻滞。β-榄香烯降低了SGC7901胃癌细胞Bcl-2蛋白表达水平,增加了Bax和活化的Caspase-3(17Kd)表达水平。β-榄香烯对SGC7901胃癌细胞Pak1(p21-activated protein kinase 1)的总蛋白表达无明显影响,但降低了Pak1(Thr423)和ERK1/2(Extracellular signal-Regulated Kinase 1/2)的磷酸化水平。结论β-榄香烯抑制胃癌细胞增殖,诱导胃癌细胞凋亡,其可能的分子机制为抑制Pak1/ERK信号通路的活化、调控Bcl-2和Bax等凋亡相关蛋白表达。
目的:探討β-欖香烯對胃癌細胞增殖和凋亡的影響及其可能的分子機製。方法通過四甲基偶氮唑鹽比色法(MTT)、流式細胞術檢測細胞凋亡、週期分佈和平闆剋隆形成實驗檢測β-欖香烯對SGC7901胃癌細胞的影響,同時評價β-欖香烯對正常胃黏膜上皮細胞GES-1的毒性作用;通過Western blots檢測β-欖香烯對SGC7901胃癌細胞的蛋白錶達影響。結果β-欖香烯顯著抑製SGC7901胃癌細胞的活性併誘導細胞凋亡,兩種作用在正常胃黏膜上皮細胞GES-1中明顯減弱。β-欖香烯降低SGC7901胃癌細胞剋隆形成率,誘導SGC7901細胞髮生G2/M期阻滯。β-欖香烯降低瞭SGC7901胃癌細胞Bcl-2蛋白錶達水平,增加瞭Bax和活化的Caspase-3(17Kd)錶達水平。β-欖香烯對SGC7901胃癌細胞Pak1(p21-activated protein kinase 1)的總蛋白錶達無明顯影響,但降低瞭Pak1(Thr423)和ERK1/2(Extracellular signal-Regulated Kinase 1/2)的燐痠化水平。結論β-欖香烯抑製胃癌細胞增殖,誘導胃癌細胞凋亡,其可能的分子機製為抑製Pak1/ERK信號通路的活化、調控Bcl-2和Bax等凋亡相關蛋白錶達。
목적:탐토β-람향희대위암세포증식화조망적영향급기가능적분자궤제。방법통과사갑기우담서염비색법(MTT)、류식세포술검측세포조망、주기분포화평판극륭형성실험검측β-람향희대SGC7901위암세포적영향,동시평개β-람향희대정상위점막상피세포GES-1적독성작용;통과Western blots검측β-람향희대SGC7901위암세포적단백표체영향。결과β-람향희현저억제SGC7901위암세포적활성병유도세포조망,량충작용재정상위점막상피세포GES-1중명현감약。β-람향희강저SGC7901위암세포극륭형성솔,유도SGC7901세포발생G2/M기조체。β-람향희강저료SGC7901위암세포Bcl-2단백표체수평,증가료Bax화활화적Caspase-3(17Kd)표체수평。β-람향희대SGC7901위암세포Pak1(p21-activated protein kinase 1)적총단백표체무명현영향,단강저료Pak1(Thr423)화ERK1/2(Extracellular signal-Regulated Kinase 1/2)적린산화수평。결론β-람향희억제위암세포증식,유도위암세포조망,기가능적분자궤제위억제Pak1/ERK신호통로적활화、조공Bcl-2화Bax등조망상관단백표체。
Objective To investigate the effects ofβ-elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms. Methods Using MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects ofβ-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES-1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response toβ-elemene treatment. Resultsβ-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells.β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl-2, and increased the expression of Bax and cleaved caspase-3. β-elemene did not obviously affect the expression of total p21-activated protein kinase 1 (Pak1) but decreased the level of phospho-Pak1 (Thr423) and phospho-ERK1/2 (Thr202/Tyr204) in SGC7901 cells. Conclusion β-elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.