中国生化药物杂志
中國生化藥物雜誌
중국생화약물잡지
CHINESE JOURNAL OF BIOCHEMICAL PHARMACEUTICS
2014年
3期
16-18
,共3页
王迎春%哈敏文%王彦%刘维%李满
王迎春%哈敏文%王彥%劉維%李滿
왕영춘%합민문%왕언%류유%리만
5-氮杂-2'-脱氧胞苷%胰腺癌%PCDH8基因
5-氮雜-2'-脫氧胞苷%胰腺癌%PCDH8基因
5-담잡-2'-탈양포감%이선암%PCDH8기인
5-Aza-CdR%pancreatic carcinoma%PCDH8 gene
目的:探讨5-氮杂-2'-脱氧胞苷(5-Aza-2'-deoxycytidine,5-Aza-CdR)对胰腺癌细胞株增殖的影响以及对其原钙黏附素(protocadherin 8,PCDH8)基因表达的影响。方法用不同浓度的5-Aza-CdR处理胰腺癌Capan-2细胞。阴性对照组不加药,根据5-Aza-CdR处理的剂量分为:0.08μmol/L组、0.40μmol/L组、2.00μmol/L组、10μmol/L组、50μmol/L组,检测细胞的生长情况;采用RT-PCR和Western Blot检测各组胰腺癌细胞PCDH8基因和蛋白的表达。结果5-Aza-CdR对胰腺癌细胞具有明显的抑制作用,且随着浓度的增加,抑制率逐渐增强(P<0.01);但是随着时间的增加,抑制率逐渐下降(P<0.01)。5-Aza-CdR和吉西他滨联用对胰腺癌细胞的抑制作用和诱导凋亡作用最强(P<0.05,P<0.01)。5-Aza-CdR能显著增加胰腺癌细胞PCDH8基因和PCDH8蛋白的表达水平,且随着浓度的升高,增加作用越明显(P<0.01)。结论5-Aza-CdR能够抑制胰腺癌细胞的增殖,增加PCDH8基因的表达,与吉西他滨联合后抑制作用更强。
目的:探討5-氮雜-2'-脫氧胞苷(5-Aza-2'-deoxycytidine,5-Aza-CdR)對胰腺癌細胞株增殖的影響以及對其原鈣黏附素(protocadherin 8,PCDH8)基因錶達的影響。方法用不同濃度的5-Aza-CdR處理胰腺癌Capan-2細胞。陰性對照組不加藥,根據5-Aza-CdR處理的劑量分為:0.08μmol/L組、0.40μmol/L組、2.00μmol/L組、10μmol/L組、50μmol/L組,檢測細胞的生長情況;採用RT-PCR和Western Blot檢測各組胰腺癌細胞PCDH8基因和蛋白的錶達。結果5-Aza-CdR對胰腺癌細胞具有明顯的抑製作用,且隨著濃度的增加,抑製率逐漸增彊(P<0.01);但是隨著時間的增加,抑製率逐漸下降(P<0.01)。5-Aza-CdR和吉西他濱聯用對胰腺癌細胞的抑製作用和誘導凋亡作用最彊(P<0.05,P<0.01)。5-Aza-CdR能顯著增加胰腺癌細胞PCDH8基因和PCDH8蛋白的錶達水平,且隨著濃度的升高,增加作用越明顯(P<0.01)。結論5-Aza-CdR能夠抑製胰腺癌細胞的增殖,增加PCDH8基因的錶達,與吉西他濱聯閤後抑製作用更彊。
목적:탐토5-담잡-2'-탈양포감(5-Aza-2'-deoxycytidine,5-Aza-CdR)대이선암세포주증식적영향이급대기원개점부소(protocadherin 8,PCDH8)기인표체적영향。방법용불동농도적5-Aza-CdR처리이선암Capan-2세포。음성대조조불가약,근거5-Aza-CdR처리적제량분위:0.08μmol/L조、0.40μmol/L조、2.00μmol/L조、10μmol/L조、50μmol/L조,검측세포적생장정황;채용RT-PCR화Western Blot검측각조이선암세포PCDH8기인화단백적표체。결과5-Aza-CdR대이선암세포구유명현적억제작용,차수착농도적증가,억제솔축점증강(P<0.01);단시수착시간적증가,억제솔축점하강(P<0.01)。5-Aza-CdR화길서타빈련용대이선암세포적억제작용화유도조망작용최강(P<0.05,P<0.01)。5-Aza-CdR능현저증가이선암세포PCDH8기인화PCDH8단백적표체수평,차수착농도적승고,증가작용월명현(P<0.01)。결론5-Aza-CdR능구억제이선암세포적증식,증가PCDH8기인적표체,여길서타빈연합후억제작용경강。
Objective To discuss the effect of 5-Aza-CdR on pancreatic carcinoma Capan-2 cell proliferation and PCDH8 gene expression.Methods Pancreatic carcinoma Capan-2 cells were treated with different doses of 5-Aza-CdR with or without gemcitabine,negative control group without drug,0.08μmol/L group with 0.08μmol/L 5-Aza-CdR,0.40 μmol/L group with 0.40 μmol/L 5-Aza-CdR,2.00 μmol/L group with 2.00 μmol/L 5-Aza-CdR,10 μmol/L group with 10 μmol/L 5-Aza-CdR,50 μmol/L group with 50 μmol/L 5-Aza-CdR. The inhibition ratio of Capan-2 cell proliferation were observed by MTT assay and PCDH8 gene and protein expression were detected by RT-PCR and Western blot. Results The inhibition ratio was increased with 5-Aza-CdR dose increasing(P<0.01),but decreased apparently with times extending(P<0.01). Inhibition ratio in 5-Aza-CdR and gemcitabine group was higher than those with only 5-Aza-CdR or gemcitabine groups(P<0.05 or P<0.01).The levels of PCDH8 gene and protein expression were increased significantly in 5-Aza-CdR treatment groups,with dose dependent (P <0.01 ).Conclusion 5-Aza-CdR can inhibit the proliferation of pancreatic carcinoma Capan-2 cell proliferation,and increase PCDH8 gene expression. The inhibition effect is strong when combined with gemcitabine.