In the current study, the antimigratory and antiproliferative effect of three substituted triazole-chelated iridium(III) complexes Ir-TRN, Ir-TRH, and Ir-TRF were studied with special emphasis on modulation of P53 activity, a cell cycle regulator. ERK2/MAPK, another crucial cell signaling pathway protein, was also shown to play a crucial role in cell migration and proliferation. The complexes increase the ROS generation within the cell, further supporting apoptotic induction by exerting cellular oxidative stress. These metal complexes also affect ER stress by altering ERp29, an ER-resident chaperone, further inducing the process of apoptosis. The iridium(III) complexes restrict cervical cancer cell migration and proliferation by exerting pronounced effects as P53 activators and downregulation of ERK2/MAPK activity in cervical cancer cells. The underpinning mechanism of P53 and ERK2/MAPK activity in cervical cancer cells in the presence of iridium(III) complexes was studied in detail in this study, which paves the way for developing promising avenues for cancer therapeutics.

中文翻译：

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泛促细胞信号通路在宫颈癌细胞中三唑螯合铱 （III） 复合物抗迁移和抗增殖作用中的调节作用


在本研究中，研究了三种取代的三唑-螯合铱 （III） 复合物 Ir-TRN、Ir-TRH 和 Ir-TRF 的抗迁移和抗增殖作用，特别强调细胞周期调节因子 P53 活性的调节。ERK2/MAPK 是另一种重要的细胞信号通路蛋白，也被证明在细胞迁移和增殖中起关键作用。复合物增加细胞内 ROS 的产生，通过施加细胞氧化应激进一步支持凋亡诱导。这些金属复合物还通过改变 ERp29（一种驻留在 ER 中的伴侣）来影响 ER 应激，从而进一步诱导细胞凋亡过程。铱 （III） 复合物通过发挥 P53 激活剂的显着作用和下调宫颈癌细胞中 ERK2/MAPK 活性来限制宫颈癌细胞的迁移和增殖。本研究详细研究了铱 （III） 复合物存在下宫颈癌细胞中 P53 和 ERK2/MAPK 活性的基础机制，为开发有前途的癌症治疗途径铺平了道路。