The androgen receptor(AR) signaling pathway plays a crucial role in the development and growth of prostate *** of AR homeostasis in prostate tumorigenesis has not yet been fully *** the present study,we demonstrate th...
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The androgen receptor(AR) signaling pathway plays a crucial role in the development and growth of prostate *** of AR homeostasis in prostate tumorigenesis has not yet been fully *** the present study,we demonstrate that p21-activated kinase 6(PAK6) inhibits prostate tumorigenesis by regulating AR ***,we demonstrated that in normal prostate epithelium,
The androgen receptor (AR) signaling pathway plays a crucial role in the development and growth of prostate *** of AR homeostasis in prostate tumorigenesis has not yet been fully characterized.
The androgen receptor (AR) signaling pathway plays a crucial role in the development and growth of prostate *** of AR homeostasis in prostate tumorigenesis has not yet been fully characterized.
目的:探讨5-氮杂-2’-脱氧胞苷对乳腺癌细胞自噬的影响及其可能的机制。方法:用依托泊苷、顺铂和5-氮杂-2’-脱氧胞苷处理乳腺癌细胞后,采用彗星实验测定细胞DNA损伤,蛋白质印迹法检测p53和p21蛋白表达;细胞自噬测定用3种方法:(1)蛋白质印迹法检测微管相关蛋白1轻链3-Ⅱ(microtubule-associated protein 1 light chain3-Ⅱ,LC3-Ⅱ)蛋白的表达;(2)用单丹磺酰戊二胺对乳腺癌细胞染色后,在荧光显微镜下计数自噬泡阳性细胞,并计算自噬泡阳性细胞百分比;(3)将pEGFP-LC3质粒转染至乳腺癌细胞后,在荧光显微镜下计数含绿色荧光蛋白的阳性细胞,并计算绿色荧光蛋白阳性细胞的百分比。结果:依托泊苷和顺铂均可诱导乳腺癌细胞DNA损伤和自噬,与对照组比较,药物处理组细胞的彗星长度增长(P<0.01),p53、p21和LC3-Ⅱ蛋白表达上调。5-氮杂-2’-脱氧胞苷也可诱导乳腺癌细胞DNA损伤和自噬,与对照组比较,处理组细胞的彗星长度增长(P<0.01),p53、p21和LC3-Ⅱ蛋白表达上调,自噬泡阳性细胞百分比和绿色荧光蛋白阳性细胞百分比上升,差异均有统计学意义(P<0.05和P<0.01)。结论:5-氮杂-2’-脱氧胞苷可诱导乳腺癌细胞自噬,其机制可能与其所诱导的DNA损伤有关。
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