RUNX2是一种关键的转录因子,其在多种癌症的发生和发展中起着重要作用。由于RUNX2在多种癌症类型中对预后具有显著的影响,其作为癌症生物标志物的潜力引起了广泛关注。RUNX2通过与核心结合因子β (CBFβ)结合,增强对靶基因的调控,促进...RUNX2是一种关键的转录因子,其在多种癌症的发生和发展中起着重要作用。由于RUNX2在多种癌症类型中对预后具有显著的影响,其作为癌症生物标志物的潜力引起了广泛关注。RUNX2通过与核心结合因子β (CBFβ)结合,增强对靶基因的调控,促进癌细胞的增殖、迁移和侵袭。RUNX2与PI3K/AKT信号通路互作,激活肿瘤进展的关键途径。抑制RUNX2的表达和功能已显示出抑制肿瘤生长和迁移、促进癌细胞凋亡的潜力,使其成为癌症治疗中的有意义靶标。近年研究还发现,RUNX2影响肿瘤微环境和化疗耐药性,针对RUNX2的小分子抑制剂和靶向疗法的开发,为提高治疗效果和减少耐药现象提供了新的策略。RUNX2 is a critical transcription factor that plays an important role in the initiation and progression of various cancers. Due to its significant impact on prognosis across multiple cancer types, RUNX2 has garnered widespread attention as a potential biomarker for cancer. By interacting with core-binding factor β (CBFβ), RUNX2 enhances the regulation of target genes, promoting cancer cell proliferation, migration, and invasion. RUNX2 also interacts with the PI3K/AKT signaling pathway, activating key pathways involved in tumor progression. Inhibiting RUNX2 expression and function has demonstrated potential in suppressing tumor growth and migration, as well as inducing apoptosis in cancer cells, making it a meaningful therapeutic target in cancer treatment. Recent studies have also revealed that RUNX2 influences the tumor microenvironment and chemotherapy resistance. The development of small molecule inhibitors and targeted therapies against RUNX2 offers novel strategies to improve therapeutic efficacy and reduce resistance.展开更多
目的基于骨组织Runx2、Osterix启动子甲基化水平,探究鹿茸中药复方对去卵巢骨质疏松症大鼠的疗效机制。方法去卵巢复制绝经后骨质疏松症(Postmenopausal Osteoporosis,PMOP)大鼠模型,将其分4组,分别为:正常组、模型组、鹿茸中药复方组...目的基于骨组织Runx2、Osterix启动子甲基化水平,探究鹿茸中药复方对去卵巢骨质疏松症大鼠的疗效机制。方法去卵巢复制绝经后骨质疏松症(Postmenopausal Osteoporosis,PMOP)大鼠模型,将其分4组,分别为:正常组、模型组、鹿茸中药复方组、仙灵骨葆阳性对照组。灌胃14周后,X射线吸收测量法检测骨密度、质谱法检测Runx2、Osterix启动子甲基化水平。结果(1)与正常组比较,模型组第1~6腰椎骨密度明显降低(P<0.01);骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG2甲基化水平明显升高(P<0.05);骨组织Osterix启动子-1082 bp^-583 bp CpG1、CpG2甲基化水平明显升高(P<0.01)。(2)与模型组比较,鹿茸中药复方组、仙灵骨葆阳性对照组第1~6腰椎骨密度明显升高(P<0.05);鹿茸中药复方组骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG3甲基化水平明显降低(P<0.05),Osterix启动子-1082 bp^-583bp CpG1甲基化水平明显降低(P<0.05);仙灵骨葆阳性对照组骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG2甲基化水平明显降低(P<0.05),Osterix启动子-1082 bp^-583 bp CpG1、CpG2甲基化水平明显降低(P<0.01)。结论鹿茸中药复方通过降低骨组织Runx2、Osterix启动子甲基化水平的表观遗传学机制,有效防治PMOP。展开更多
文摘RUNX2是一种关键的转录因子,其在多种癌症的发生和发展中起着重要作用。由于RUNX2在多种癌症类型中对预后具有显著的影响,其作为癌症生物标志物的潜力引起了广泛关注。RUNX2通过与核心结合因子β (CBFβ)结合,增强对靶基因的调控,促进癌细胞的增殖、迁移和侵袭。RUNX2与PI3K/AKT信号通路互作,激活肿瘤进展的关键途径。抑制RUNX2的表达和功能已显示出抑制肿瘤生长和迁移、促进癌细胞凋亡的潜力,使其成为癌症治疗中的有意义靶标。近年研究还发现,RUNX2影响肿瘤微环境和化疗耐药性,针对RUNX2的小分子抑制剂和靶向疗法的开发,为提高治疗效果和减少耐药现象提供了新的策略。RUNX2 is a critical transcription factor that plays an important role in the initiation and progression of various cancers. Due to its significant impact on prognosis across multiple cancer types, RUNX2 has garnered widespread attention as a potential biomarker for cancer. By interacting with core-binding factor β (CBFβ), RUNX2 enhances the regulation of target genes, promoting cancer cell proliferation, migration, and invasion. RUNX2 also interacts with the PI3K/AKT signaling pathway, activating key pathways involved in tumor progression. Inhibiting RUNX2 expression and function has demonstrated potential in suppressing tumor growth and migration, as well as inducing apoptosis in cancer cells, making it a meaningful therapeutic target in cancer treatment. Recent studies have also revealed that RUNX2 influences the tumor microenvironment and chemotherapy resistance. The development of small molecule inhibitors and targeted therapies against RUNX2 offers novel strategies to improve therapeutic efficacy and reduce resistance.
文摘目的基于骨组织Runx2、Osterix启动子甲基化水平,探究鹿茸中药复方对去卵巢骨质疏松症大鼠的疗效机制。方法去卵巢复制绝经后骨质疏松症(Postmenopausal Osteoporosis,PMOP)大鼠模型,将其分4组,分别为:正常组、模型组、鹿茸中药复方组、仙灵骨葆阳性对照组。灌胃14周后,X射线吸收测量法检测骨密度、质谱法检测Runx2、Osterix启动子甲基化水平。结果(1)与正常组比较,模型组第1~6腰椎骨密度明显降低(P<0.01);骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG2甲基化水平明显升高(P<0.05);骨组织Osterix启动子-1082 bp^-583 bp CpG1、CpG2甲基化水平明显升高(P<0.01)。(2)与模型组比较,鹿茸中药复方组、仙灵骨葆阳性对照组第1~6腰椎骨密度明显升高(P<0.05);鹿茸中药复方组骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG3甲基化水平明显降低(P<0.05),Osterix启动子-1082 bp^-583bp CpG1甲基化水平明显降低(P<0.05);仙灵骨葆阳性对照组骨组织Runx2启动子-955 bp^-456 bp CpG1、CpG2甲基化水平明显降低(P<0.05),Osterix启动子-1082 bp^-583 bp CpG1、CpG2甲基化水平明显降低(P<0.01)。结论鹿茸中药复方通过降低骨组织Runx2、Osterix启动子甲基化水平的表观遗传学机制,有效防治PMOP。
