宫颈癌的发展主要归因于高危人类乳头状瘤病毒(HR-HPVs)的感染。近年来发现HPV阳性宫颈癌的恶性生物学行为考虑可能为氧化应激环境的作用促进了病毒对宫颈鳞状上皮组织慢性感染所致的持续病变。抗氧化应激核心途径中的核转录因子E2相关...宫颈癌的发展主要归因于高危人类乳头状瘤病毒(HR-HPVs)的感染。近年来发现HPV阳性宫颈癌的恶性生物学行为考虑可能为氧化应激环境的作用促进了病毒对宫颈鳞状上皮组织慢性感染所致的持续病变。抗氧化应激核心途径中的核转录因子E2相关因子2 (Nrf2)和Kelch样ech相关蛋白1 (Keap1)成分对于稳定内环境至关重要。肿瘤的发展与Nrf2的过度激活有很大关联,而这一激活则引导了一系列涉及赋予肿瘤恶化特性自我增殖、迁移、调控基因的表达。Nrf2因具有多面性功能,研究者正尝试通过抑制Keap1-Nrf2-抗氧化反应元件(ARE)路径,来发展针对性癌症治疗方法。进行临床研究对相关靶点设计进一步的治疗方案,对宫颈癌治疗预后进展至关重要。Cervical carcinoma advancement is primarily linked to the presence of oncogenic human papillomavirus (HPV) types. Recent investigations suggest the neoplastic activities associated with HPV-positive cervical neoplasms could stem from oxidative stress, which drives prolonged pathological transformation in the cervix’s epithelium as a consequence of continuous viral onslaught. The Nrf2/Keap1 signaling pathway is a key molecule regulating oxidative stress. The Nrf2 protein is activated in tumors, and activated Nrf2 participates in malignant biological behaviors such as tumor cell replication, implantation, and invasion after being activated by multiple target genes. Modulating the interaction among Keap1, Nrf2, and the antioxidant response element (ARE) is increasingly recognized as an elaborate approach in cancer therapy, given Nrf2’s complex regulatory effects. Advancing clinical investigations to devise sophisticated therapeutic strategies targeting specific molecules is imperative for enhancing the treatment outcomes of cervical carcinoma.展开更多
文摘宫颈癌的发展主要归因于高危人类乳头状瘤病毒(HR-HPVs)的感染。近年来发现HPV阳性宫颈癌的恶性生物学行为考虑可能为氧化应激环境的作用促进了病毒对宫颈鳞状上皮组织慢性感染所致的持续病变。抗氧化应激核心途径中的核转录因子E2相关因子2 (Nrf2)和Kelch样ech相关蛋白1 (Keap1)成分对于稳定内环境至关重要。肿瘤的发展与Nrf2的过度激活有很大关联,而这一激活则引导了一系列涉及赋予肿瘤恶化特性自我增殖、迁移、调控基因的表达。Nrf2因具有多面性功能,研究者正尝试通过抑制Keap1-Nrf2-抗氧化反应元件(ARE)路径,来发展针对性癌症治疗方法。进行临床研究对相关靶点设计进一步的治疗方案,对宫颈癌治疗预后进展至关重要。Cervical carcinoma advancement is primarily linked to the presence of oncogenic human papillomavirus (HPV) types. Recent investigations suggest the neoplastic activities associated with HPV-positive cervical neoplasms could stem from oxidative stress, which drives prolonged pathological transformation in the cervix’s epithelium as a consequence of continuous viral onslaught. The Nrf2/Keap1 signaling pathway is a key molecule regulating oxidative stress. The Nrf2 protein is activated in tumors, and activated Nrf2 participates in malignant biological behaviors such as tumor cell replication, implantation, and invasion after being activated by multiple target genes. Modulating the interaction among Keap1, Nrf2, and the antioxidant response element (ARE) is increasingly recognized as an elaborate approach in cancer therapy, given Nrf2’s complex regulatory effects. Advancing clinical investigations to devise sophisticated therapeutic strategies targeting specific molecules is imperative for enhancing the treatment outcomes of cervical carcinoma.
