中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2010年
5期
338-340
,共3页
程宪永%熊光苏%李祥苏%吴叔明
程憲永%熊光囌%李祥囌%吳叔明
정헌영%웅광소%리상소%오숙명
胰腺肿瘤%吉西他滨%Notch受体%信号转导
胰腺腫瘤%吉西他濱%Notch受體%信號轉導
이선종류%길서타빈%Notch수체%신호전도
Pancreatic neoplasms%Gemcitabine%Notch receptors%Signal transducing
目的 观察吉西他滨对人胰腺癌细胞(SW1990和BxPC3)Notch信号通路活性的影响,探讨其与胰腺癌对吉西他滨化疗耐药的关系.方法 不同浓度吉西他滨处理人胰腺癌SW1990和BxPC3细胞株48 h,实时定量PCR检测Notch信号通路受体Notch1、2、3、4,配体Jagged1、2和下游靶基因Hes1 mRNA的表达,Western blotting测定细胞Hes1蛋白表达.结果 2μmol/L吉西他滨作用胰腺癌细胞株48 h,SW1990细胞的Notch1、2、3、Jagged1、2和Hes1 mRNA表达量分别为8.26±0.48、39.12±4.87、0.84±0.06、105.8±17.92、6.59±0.32和17.30±2.96,均较未处理细胞的1.02±0.15、15.25±1.28、0.12±0.02、32.66±1.98、1.88±0.29和5.02±0.64明显升高(P<0.05或P<0.01);BxPC3细胞上述各项表达量分别为7.87±0.59、109.4±10.98、0.74±0.19、62.73±13.50、2.09±0.16和15.38±1.06,也均较未处理细胞的1.14±0.43、58.96±2.63、0.10±0.02、16.95±3.79、0.98±0.02和2.04±0.16,明显升高(P<0.05或P<0.01).1、2 μmol/L吉西他滨作用胰腺癌细胞株48 h,SW1990细胞Hes1蛋白表达量分别为0.30±0.03、0.42±0.03;BxPC3细胞分别为0.33±0.02、0.45±0.03,均较未处理细胞显著增高(0.13±0.01、F=33.71;0.09±0.02、F=38.54,P值均<0.01).结论 吉西他滨可明显激活SW1990和BxPC3细胞的Notch信号通路,这可能是胰腺癌细胞获得化疗耐受性的机制之一.
目的 觀察吉西他濱對人胰腺癌細胞(SW1990和BxPC3)Notch信號通路活性的影響,探討其與胰腺癌對吉西他濱化療耐藥的關繫.方法 不同濃度吉西他濱處理人胰腺癌SW1990和BxPC3細胞株48 h,實時定量PCR檢測Notch信號通路受體Notch1、2、3、4,配體Jagged1、2和下遊靶基因Hes1 mRNA的錶達,Western blotting測定細胞Hes1蛋白錶達.結果 2μmol/L吉西他濱作用胰腺癌細胞株48 h,SW1990細胞的Notch1、2、3、Jagged1、2和Hes1 mRNA錶達量分彆為8.26±0.48、39.12±4.87、0.84±0.06、105.8±17.92、6.59±0.32和17.30±2.96,均較未處理細胞的1.02±0.15、15.25±1.28、0.12±0.02、32.66±1.98、1.88±0.29和5.02±0.64明顯升高(P<0.05或P<0.01);BxPC3細胞上述各項錶達量分彆為7.87±0.59、109.4±10.98、0.74±0.19、62.73±13.50、2.09±0.16和15.38±1.06,也均較未處理細胞的1.14±0.43、58.96±2.63、0.10±0.02、16.95±3.79、0.98±0.02和2.04±0.16,明顯升高(P<0.05或P<0.01).1、2 μmol/L吉西他濱作用胰腺癌細胞株48 h,SW1990細胞Hes1蛋白錶達量分彆為0.30±0.03、0.42±0.03;BxPC3細胞分彆為0.33±0.02、0.45±0.03,均較未處理細胞顯著增高(0.13±0.01、F=33.71;0.09±0.02、F=38.54,P值均<0.01).結論 吉西他濱可明顯激活SW1990和BxPC3細胞的Notch信號通路,這可能是胰腺癌細胞穫得化療耐受性的機製之一.
목적 관찰길서타빈대인이선암세포(SW1990화BxPC3)Notch신호통로활성적영향,탐토기여이선암대길서타빈화료내약적관계.방법 불동농도길서타빈처리인이선암SW1990화BxPC3세포주48 h,실시정량PCR검측Notch신호통로수체Notch1、2、3、4,배체Jagged1、2화하유파기인Hes1 mRNA적표체,Western blotting측정세포Hes1단백표체.결과 2μmol/L길서타빈작용이선암세포주48 h,SW1990세포적Notch1、2、3、Jagged1、2화Hes1 mRNA표체량분별위8.26±0.48、39.12±4.87、0.84±0.06、105.8±17.92、6.59±0.32화17.30±2.96,균교미처리세포적1.02±0.15、15.25±1.28、0.12±0.02、32.66±1.98、1.88±0.29화5.02±0.64명현승고(P<0.05혹P<0.01);BxPC3세포상술각항표체량분별위7.87±0.59、109.4±10.98、0.74±0.19、62.73±13.50、2.09±0.16화15.38±1.06,야균교미처리세포적1.14±0.43、58.96±2.63、0.10±0.02、16.95±3.79、0.98±0.02화2.04±0.16,명현승고(P<0.05혹P<0.01).1、2 μmol/L길서타빈작용이선암세포주48 h,SW1990세포Hes1단백표체량분별위0.30±0.03、0.42±0.03;BxPC3세포분별위0.33±0.02、0.45±0.03,균교미처리세포현저증고(0.13±0.01、F=33.71;0.09±0.02、F=38.54,P치균<0.01).결론 길서타빈가명현격활SW1990화BxPC3세포적Notch신호통로,저가능시이선암세포획득화료내수성적궤제지일.
Objective To investigate the changes of Notch signaling pathway activity in human pancreatic cancer cell lines (SW1990, BxPC3 )after gemcitabine induction, and to study its relationship with pancreatic cancer resistant to gemcitabine chemotherapy. Methods The pancreatic cancer cell lines SW1990 and BxPC3 were cultured with different concentrations of gemcitabine for 48 hours. The Notch signaling pathway receptors ( Notch1, Notch2, Notch3, Notch4), ligands (Jagged1, Jagged2) and downstream target Hesl mRNAs expression were detected by quantitative real-time PCR (Q-PCR). Protein levels of Hes1 were determined by Western blotting. Results After treatment with 2 μmol/L gemcitabine for 48 hours, the expression of Notch1, Notch2, Notch3, Jagged1, Jagged2 and Hes1 mRNAs in SW1990 cells were 8.26 ±0.48, 39.12 ±4.87, 0.84 ±0.06, 105.8 ± 17.92, 6.59 ±0.32 and 17.30 ±2.96, which were significantly elevated when compared with those without gemcitabine treatment ( 1.02 ± 0. 15, 15.25 ± 1.28, 0. 12 ± 0.02,32.66 ± 1.98, 1.88 ± 0.29 and 5.02 ± 0.64, P < 0.05 or P < 0. 01 ); the expression in BxPC3 cells was 7.87 ±0.59, 109.4 ± 10.98, 0.74 ±0.19, 62.73 ± 13.50, 2.09 ±0.16 and 15.38 ± 1.06, which were significantly elevated when compared with those without gemcitabine treatment ( 1.14 ±0.43, 58.96 ±2.63,0.10 ± 0.02, 16.95 ± 3.79, 0.98 ± 0.02 and 2.04 ± 0.16, P < 0.05 or P < 0.01 ). The expressions of Hes1protein in SW1990 cells after 1, 2 μmol/L gemcitabine treatment for 48 h were 0.30 ±0.03, 0.42 ±0.03;and the expressions in BxPC3 cells were 0.33 ± 0.02, 0.45 ± 0.03, which were significantly increased when compared with those without gemcitabine treatment (0.13 ± 0.01, F = 33.71,0.09 ± 0.02, F = 38.54, P <0.01 ). Conclusions The Notch signaling pathway is significantly activated in pancreatic cancer cells SW1990 and BxPC3 by gemcitabine, which may be one of the mechanisms of chemoresistance.
