[目的]探究miR-325-3p靶向PRDX4对肾细胞癌细胞增殖、侵袭及凋亡的影响。[方法]设肾细胞癌细胞Caki-1组、miR-NC组、miR-325-3p-mimics组(过表达)、miR-325-3p-inhibitor组(低表达),测定各组细胞增殖、单克隆形成数目、凋亡率、侵袭水...[目的]探究miR-325-3p靶向PRDX4对肾细胞癌细胞增殖、侵袭及凋亡的影响。[方法]设肾细胞癌细胞Caki-1组、miR-NC组、miR-325-3p-mimics组(过表达)、miR-325-3p-inhibitor组(低表达),测定各组细胞增殖、单克隆形成数目、凋亡率、侵袭水平以及miR-325-3p、PRDX4水平。[结果]miR-325-3p-inhibitor组OD值(0.93±0.03)、存活率(86.58±6.36)%、单克隆形成数目(1062.29±102.78)、穿膜数(1917.34±425.35)、PRDX4 mRNA和蛋白表达水平(4.63±0.28、1.82±0.18)高于miR-325-3p-mimics组[(0.42±0.02)、(42.25±7.20)%、(239.89±35.27)个、(293.85±95.28)个、(2.04±0.24)、(0.38±0.07)](P<0.05),细胞凋亡率(1.12±0.29)%、miR-325-3p表达水平(1.42±0.38)低于miR-325-3p-mimics组(7.14±1.11)%、(5.68±0.37)(P<0.05)。[结论]miR-325-3p上调可以抑制肾细胞癌细胞的增殖(76.59%±7.30%vs 42.25%±7.20%)、迁移侵袭(702.28±111.52 vs 293.85±95.28),同时诱导细胞凋亡(3.46±1.04 vs 7.14±1.11),而这些过程主要是通过miR-325-3p与PRDX4的相互作用实现的。展开更多
Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmen...Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmental endocrine disruptor,in the serum and skin of captive FMDs.Feeding FMDs with maslinic acid(MA)has been observed to alleviate the stress response and improve reproductive rates,although the precise molecular mechanisms remain unclear.Therefore,this study aims to investigate the molecular mechanisms underlying the alleviation of DEHP-induced oxidative stress and cell apoptosis in primary peritubular myoid cells(PMCs)through MA intake.Primary PMCs were isolated and exposed to DEHP in vitro.The results demonstrated that DEHP significantly suppressed antioxidant levels and promoted cell apoptosis in primary PMCs.Moreover,interfering with the expression of PRDX6 was found to induce excessive reactive oxygen species(ROS)production and cell apoptosis in primary PMCs.Supplementation with MA significantly upregulated the expression of PRDX6,thereby attenuating DEHP-induced oxidative stress and cell apoptosis in primary PMCs.These findings provide a theoretical foundation for mitigating stress levels and enhancing reproductive capacity of in captive FMDs.展开更多
文摘[目的]探究miR-325-3p靶向PRDX4对肾细胞癌细胞增殖、侵袭及凋亡的影响。[方法]设肾细胞癌细胞Caki-1组、miR-NC组、miR-325-3p-mimics组(过表达)、miR-325-3p-inhibitor组(低表达),测定各组细胞增殖、单克隆形成数目、凋亡率、侵袭水平以及miR-325-3p、PRDX4水平。[结果]miR-325-3p-inhibitor组OD值(0.93±0.03)、存活率(86.58±6.36)%、单克隆形成数目(1062.29±102.78)、穿膜数(1917.34±425.35)、PRDX4 mRNA和蛋白表达水平(4.63±0.28、1.82±0.18)高于miR-325-3p-mimics组[(0.42±0.02)、(42.25±7.20)%、(239.89±35.27)个、(293.85±95.28)个、(2.04±0.24)、(0.38±0.07)](P<0.05),细胞凋亡率(1.12±0.29)%、miR-325-3p表达水平(1.42±0.38)低于miR-325-3p-mimics组(7.14±1.11)%、(5.68±0.37)(P<0.05)。[结论]miR-325-3p上调可以抑制肾细胞癌细胞的增殖(76.59%±7.30%vs 42.25%±7.20%)、迁移侵袭(702.28±111.52 vs 293.85±95.28),同时诱导细胞凋亡(3.46±1.04 vs 7.14±1.11),而这些过程主要是通过miR-325-3p与PRDX4的相互作用实现的。
基金supported by the Fund of Sci-Tech Innovation Program of Shaanxi Academy of Forestry(No.SXLK2021-0219)the Science and Technology Project of Shaanxi Province(No.2022SF-512)the Science and Technology Innovation and Achievement Transformation Project of Experimental Demonstration Station(base)of Northwest A&F University(No.TGZX2021-32)。
文摘Chinese forest musk deer(FMD),an endangered species,have exhibited low reproductive rates even in captivity due to stress conditions.Investigation revealed the presence of di(2-ethylhexyl)phthalate(DEHP),an environmental endocrine disruptor,in the serum and skin of captive FMDs.Feeding FMDs with maslinic acid(MA)has been observed to alleviate the stress response and improve reproductive rates,although the precise molecular mechanisms remain unclear.Therefore,this study aims to investigate the molecular mechanisms underlying the alleviation of DEHP-induced oxidative stress and cell apoptosis in primary peritubular myoid cells(PMCs)through MA intake.Primary PMCs were isolated and exposed to DEHP in vitro.The results demonstrated that DEHP significantly suppressed antioxidant levels and promoted cell apoptosis in primary PMCs.Moreover,interfering with the expression of PRDX6 was found to induce excessive reactive oxygen species(ROS)production and cell apoptosis in primary PMCs.Supplementation with MA significantly upregulated the expression of PRDX6,thereby attenuating DEHP-induced oxidative stress and cell apoptosis in primary PMCs.These findings provide a theoretical foundation for mitigating stress levels and enhancing reproductive capacity of in captive FMDs.
