中国医科大学学报
中國醫科大學學報
중국의과대학학보
Journal of China Medical University
2015年
10期
877-882
,共6页
郑华川%申道福%杨雪峰%勾文峰%赵爽%张文陆
鄭華川%申道福%楊雪峰%勾文峰%趙爽%張文陸
정화천%신도복%양설봉%구문봉%조상%장문륙
胃癌%BTG3%肿瘤发生%病理生物学行为%基因治疗
胃癌%BTG3%腫瘤髮生%病理生物學行為%基因治療
위암%BTG3%종류발생%병리생물학행위%기인치료
gastric cancer%BTG3%carcinogenesis%pathobiological behaviors%gene therapy
目的:研究胃癌中BTG3表达的临床病理意义,揭示BTG3对胃癌细胞恶性表型的逆转作用。方法采用联合组织芯片和免疫组化检测胃癌中BTG3表达,胃癌细胞MKN28和MGC803过表达BTG3,分别利用CCK?8、PI染色、碱性磷酸酶活性测定和GFP?LC?3B转染观察细胞增殖、细胞周期、分化和自噬。结果 BTG3过表达可以抑制胃癌细胞增殖、诱导细胞周期S/G2期阻滞、分化和自噬(P<0.05),胃癌组织中BTG3表达下调(P<0.05),BTG3表达与胃癌静脉侵袭和去分化呈正相关(P<0.05)。结论 BTG3表达下调参与胃癌发生和演进过程,BTG3过表达可以逆转胃癌恶性表型,可以作为胃癌基因治疗的潜在靶点。
目的:研究胃癌中BTG3錶達的臨床病理意義,揭示BTG3對胃癌細胞噁性錶型的逆轉作用。方法採用聯閤組織芯片和免疫組化檢測胃癌中BTG3錶達,胃癌細胞MKN28和MGC803過錶達BTG3,分彆利用CCK?8、PI染色、堿性燐痠酶活性測定和GFP?LC?3B轉染觀察細胞增殖、細胞週期、分化和自噬。結果 BTG3過錶達可以抑製胃癌細胞增殖、誘導細胞週期S/G2期阻滯、分化和自噬(P<0.05),胃癌組織中BTG3錶達下調(P<0.05),BTG3錶達與胃癌靜脈侵襲和去分化呈正相關(P<0.05)。結論 BTG3錶達下調參與胃癌髮生和縯進過程,BTG3過錶達可以逆轉胃癌噁性錶型,可以作為胃癌基因治療的潛在靶點。
목적:연구위암중BTG3표체적림상병리의의,게시BTG3대위암세포악성표형적역전작용。방법채용연합조직심편화면역조화검측위암중BTG3표체,위암세포MKN28화MGC803과표체BTG3,분별이용CCK?8、PI염색、감성린산매활성측정화GFP?LC?3B전염관찰세포증식、세포주기、분화화자서。결과 BTG3과표체가이억제위암세포증식、유도세포주기S/G2기조체、분화화자서(P<0.05),위암조직중BTG3표체하조(P<0.05),BTG3표체여위암정맥침습화거분화정정상관(P<0.05)。결론 BTG3표체하조삼여위암발생화연진과정,BTG3과표체가이역전위암악성표형,가이작위위암기인치료적잠재파점。
Objective To clarify the clinicopathological significance and the reversing effects of BTG3 expression on the aggressive phenotype in gastric cancer. Methods BTG3 expression was detected in gastric cancer tissues by on tissue microarray and immunostaining. BTG3?expressing plasmid was transfected into MKN28 and MGC803 cells,the proliferation,cell cycle,differentiation and autophagy were analyzed by CCK?8,PI staining,alkaline phosphatase activity and GFP?LC?3B transfection,respectively. Results BTG3 overexpression inhibited cell proliferation,in?duced S/G2 arrest,differentiation and autophagy in both cells(P<0.05). BTG3 expression was decreased in gastric cancer in comparison with the adjacent mucosa(P<0.05),and positively correlated with venous invasion and dedifferentiation of the cancers(P<0.05). Conclusion BTG3 ex?pression contributes to gastric carcinogenesis and subsequent progression. BTG3 overexpression can reverse the aggressive phenotypes,which could be employed as a potential target for gene therapy of gastric cancer.