Burkitt's lymphoma (BL) is the fastest growing human tumor. Current treatment consists of a multiagent regimen of cytotoxic drugs with serious side effjects including tumor lysis, cardiotoxicity, hepatic impairment, neuropathy, myelosuppression, increased susceptibility to malignancy, and death. Furthermore, therapeutic interventions in areas of BL prevalence are not as feasible as in high-income countries. Therefore, there exists an urgent need to identify new therapies with a safer profile and improved accessibility. Triclosan (TCS), an antimicrobial used in personal care products and surgical scrubs, has gained considerable interest as an antitumor agent due to its interference with fatty acid synthesis. Here, we investigate the antitumor properties and associated molecular mechanisms of TCS in BL-derived BJAB cells. Dose-dependent cell death was observed following treatment with 10–100 µM TCS for 24 h, which was associated with membrane phospholipid scrambling, compromised permeability, and cell shrinkage. TCS-induced cell death was accompanied by elevated intracellular calcium, perturbed redox balance, chromatin condensation, and DNA fragmentation. TCS upregulated Bad expression and downregulated that of Bcl2. Moreover, caspase and JNK MAPK signaling were required for the full apoptotic activity of TCS. In conclusion, this report identifies TCS as an antitumor agent and provides new insights into the molecular mechanisms governing TCS-induced apoptosis in BL cells.

伯基特淋巴瘤 (BL) 是增长最快的人类肿瘤。目前的治疗包括细胞毒性药物的多药方案，具有严重的副作用，包括肿瘤溶解、心脏毒性、肝损伤、神经病变、骨髓抑制、增加对恶性肿瘤的易感性和死亡。此外，在 BL 流行地区的治疗干预并不像在高收入国家那样可行。因此，迫切需要确定具有更安全特征和改善可及性的新疗法。三氯生 (TCS) 是一种用于个人护理产品和外科磨砂膏的抗菌剂，由于其干扰脂肪酸合成而作为抗肿瘤剂引起了广泛关注。在这里，我们研究了 TCS 在 BL 衍生的 BJAB 细胞中的抗肿瘤特性和相关的分子机制。在用 10–100 µM TCS 处理 24 小时后观察到剂量依赖性细胞死亡，这与膜磷脂扰乱、渗透性受损和细胞收缩有关。TCS 诱导的细胞死亡伴随着细胞内钙升高、氧化还原平衡紊乱、染色质浓缩和 DNA 断裂。TCS上调Bcl2表达不良并下调。此外，半胱天冬酶和 JNK MAPK 信号是 TCS 完全凋亡活性所必需的。总之，本报告将 TCS 确定为一种抗肿瘤剂，并为控制 TCS 诱导的 BL 细胞凋亡的分子机制提供了新的见解。