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铜化物复合物释放氧化,并选择性地诱导口腔癌前期和癌细胞亡

Yen-Yun Wang¹, Pang-Yu Chen², Naorem Jemes Meitei³

¹School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Drug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.

Journal of inorganic biochemistry

|January 24, 2025

概括

铜化物复合物在治疗口腔癌前期和癌症方面表现有前途. L1Cu(NO2) 通过阻止细胞循环进展和诱导细胞亡来选择性地杀死癌细胞,这表明有针对性的治疗潜力.

科学领域:

生物化学生物化学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

氧化 (NO) 是一个关键的信号分子,参与许多生理过程.
失调的NO信号与各种疾病有关,包括心血管疾病,糖尿病和癌症.
口腔癌前期和癌症代表着重要的全球健康挑战,需要新的治疗策略.

研究的目的:

研究铜化物复合体在口腔癌前期和癌症治疗中的治疗潜力.
评估新型铜-化物复合物 (L1Cu(NO2) 和L2Cu(NO2) 在细胞内释放氧化 (NO) 的能力.
评估这些复合体在口腔癌细胞中的选择性细胞毒性和潜在机制.

主要方法:

复合和表征铜-化物复合物,L1Cu(NO2) 和L2Cu(NO2).
在体外评估从癌细胞内的复合物中释放的NO.
对口腔癌前期和癌细胞系的选择性细胞毒性的评估.
细胞周期进展 (G0/G1停止) 和亡诱导的分析.
测量p-PRAS40 (富含proline的Akt基质40kDa) 的表达水平.

主要成果:

复合的铜化物有效地释放NO到口腔癌细胞中.
无论是L1Cu(NO2) 和L2Cu(NO2),都对口腔癌前和癌细胞表现出选择性细胞毒性.
通过诱导G0/G1阶段细胞循环停止,L1Cu(NO2) 显著抑制了口腔癌细胞的增殖.
L1Cu(NO2) 促进了癌细胞的亡,并上调了p-PRAS40.的表达.

结论:

铜化物复合物,特别是L1Cu(NO2),对口腔癌前期和癌症具有显著的治疗潜力.
该机制涉及选择性NO释放,导致细胞循环停止,细胞亡和关键信号通路的调节.
这些发现支持L1Cu(NO2) 作为口腔瘤学的向治疗剂的发展.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.细胞循环的细胞周期复合铜-亚酸盐复合物复合铜-亚酸盐复合物氧化氧化是什么?口腔癌是一种口腔癌.在PRAS40中,我们可以使用PRAS40的方法.

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