论文部分内容阅读
目的探讨hTERT基因全硫代修饰反义寡核苷酸(AS PS-ODN)抑制氟他胺耐受型前列腺癌细胞LNCaP-flu端粒酶活性后,藏药镰状棘豆总黄体酮(TFOF)对LNCaP-flu细胞凋亡的影响。方法采用TRAP-PCRELISA法检测氟他胺耐受型前列腺癌细胞LNCaP-flu端粒酶活性;采用台盼蓝观察hTERT AS PS-ODN与TFOF共同作用对氟他胺耐受型前列腺癌细胞LNCaP-flu生长活力的影响;通过双标流式细胞仪测定凋亡细胞的百分率。结果hTERTAS PS-ODN作用于LNCaP-flu细胞48h,端粒酶活性明显下降;hTERTAS PS-ODN作用于LNCaP-flu细胞后加入TFOF 0.1g/L作用48h,LNCaP-flu细胞的抑制率与对照组、S PS-ODN组、AS PS-ODN组、TFOF组及S PS-ODN+TFOF组相比有统计学差异(P<0.01)。hTERTAS PS-ODN作用于LNCaP-flu细胞后加入0.1g/L TFOF作用48h,凋亡细胞的百分率分别与对照组、S PS-ODN组、AS PS-ODN组、TFOF组及S PS-ODN+TFOF组相比有显著性差异(P<0.05)。结论hTER7基因反义核酸对TFOF诱导的氟他胺耐受型前列腺癌细胞LNCaP-flu凋亡有增敏作用。
Objective To investigate the effect of hTERT antisense oligodeoxynucleotide (AS PS-ODN) on the telomerase activity of LNCaP-flu in patients with famotidine-tolerant prostate cancer (TFOF ) On the apoptosis of LNCaP-flu cells. Methods The telomerase activity of LNCaP-flu in patients with famotidine-tolerant prostate cancer was detected by TRAP-PCR. The expression of LNCaP-flu in L-phenylalanine-resistant prostate cancer cells was observed by trypan blue staining. flu growth vigor; the percentage of apoptotic cells was determined by double-labeled flow cytometry. Results After treated with hTERTAS PS-ODN for 48h, the telomerase activity was significantly decreased. After treated with hTERTAS PS-ODN for 48h, TFOF 0.1g / L was added to LNCaP-flu cells for 48h. Compared with the control group , S PS-ODN group, AS PS-ODN group, TFOF group and S PS-ODN + TFOF group (P <0.01). After treated with hTERTAS PS-ODN for 48h, the percentage of apoptotic cells was significantly increased compared with control group, PS-ODN group, AS PS-ODN group, TFOF group and S PS-ODN + TFOF group was significantly different (P <0.05). Conclusion The hTER7 gene antisense oligonucleotide can sensitize TFOF-induced apoptosis of LNCaP-flu in patients with famotidine-resistant prostate cancer.