针对凋亡途径的靶向治疗被确认为治疗肺癌的一种有前景的策略。我们合成了一种新的Renieramycin T (RT) 衍生物，命名为DH_22，并在人类肺癌细胞中研究了其抗癌活性。RT衍生物DH_22是从RT进行化学修饰而得。通过挽救V-FITC/PI染色和核染色的方法评估了在A549细胞中DH_22的诱导凋亡效应。此外，还通过Western blot分析了分子途径。在细胞存活率和核染色实验中，发现DH_22具有细胞毒性，IC50为13.27 μM；它能诱导肺癌细胞凋亡。关于其机制，DH_22有助于激活依赖于p53的凋亡和降低细胞中c-Myc的水平。p53依赖机制表现为p53增加，促凋亡蛋白Bax诱导增加，抗凋亡蛋白B细胞淋巴瘤2 (Bcl-2)减少。DH_22在作为新的抗癌药物方面具有巨大的开发潜力。 版权所有 © 2023, 国际抗癌研究学院 (George J. Delinasios博士)，保留所有权利。

Targeting apoptotic pathways has been identified as a promising strategy for the treatment of lung cancer. We synthesized a new derivative of renieramycin T (RT), named DH_22, and examined its anticancer activities in human lung cancer cells.The RT derivative DH_22 was chemically modified from RT. The apoptosis-inducing effect was evaluated in A549 cells by annexin V-FITC/PI staining and nuclear staining assay (Hoechst/PI). In addition, the molecular pathway was analyzed by western blot analysis.In the cell viability and nuclear staining tests, DH_22 was discovered to be cytotoxic with an IC50 of 13.27 μM; it induced apoptosis of lung cancer cells. Regarding the mechanism, DH_22 contributed to the activation of p53-dependent apoptosis and decreased the cellular level of c-Myc. The p53-dependent mechanism was indicated by an increase in p53, an induction of the pro-apoptotic Bax protein, and a decrease in the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein.DH_22 has great potential for further development as a new anticancer drug.Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.