PTPN6通过抑制SP1/p38 MAPK信号通路促进前列腺癌细胞的化疗敏感性

PTPN6 promotes chemosensitivity of prostate cancer cells by inhibiting SP1/p38 MAPK signaling pathway

目的:研究PTPN6对前列腺癌细胞PC3的作用及其作用机制。方法:RT-PCR和Western blot实验检测前列腺癌组织和细胞以及癌旁组织和人前列腺上皮细胞中PTPN6的表达量;CCK-8和EDU染色实验检测PTPN6对前列腺癌细胞PC3增殖的影响;Western blot实验检测耐药相关蛋白P-gp和MRP-1的蛋白表达水平。结果:RT-PCR和Western blot结果显示,PTPN6在前列腺癌组织和细胞中的表达量显著低于癌旁组织和人前列腺上皮细胞中的表达量;过表达PTPN6显著抑制前列腺癌PC3细胞的增殖,并降低PC3细胞的耐药性;进一步的研究结果表明PTPN6可通过抑制SP1,并抑制p38 MAPK通路抑制PC3细胞的增殖和耐药。结论:PTPN6能够抑制前列腺癌细胞PC3的增殖和耐药,提高其化疗敏感性,作用机制是通过调控SP1/p38 MAPK信号通路来实现的,这一结果能够为临床上前列腺癌的诊断和治疗提供分子基础。

Objective:To study the effect and mechanism of PTPN6 on prostate cancer cell line PC3.Methods:RT-PCR and Western blot were used to detect the expression of PTPN6 in prostate cancer tissues and cells,as well as in adjacent tissues and prostatic epithelial cells.CCK-8 and EDU staining were used to detect the effect of PTPN6 on the proliferation of prostate cancer cell PC3.Western blot was used to detect the expression of P-gp and MRP-1.Results:The results of RT-PCR and Western blot showed that the expression of PTPN6 in prostate cancer tissues and cells was significantly lower than that in adjacent tissues and prostatic epithelial cells.Overexpression of PTPN6 significantly inhibited the proliferation of prostate cancer PC3 and decreased the drug resistance of PC3 cells.Further research showed that PTPN6 inhibited the proliferation and drug resistance of PC3 cells by inhibiting SP1 and p38 MAPK pathway.Conclusion:PTPN6 inhibited the proliferation and drug resistance of prostate cancer cell line PC3,and improve its chemotherapeutic sensitivity.Its mechanism is through the regulation of SP1/p38 MAPK signal pathway.These results provide a molecular basis for clinical diagnosis and treatment of prostate cancer.