Department of Biological Science and Technology, China Medical University, Taichung 406040, Taiwan, R.O.C.
Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404332, Taiwan, R.O.C.
J Pharm Pharmacol. 2022 Sep 1;74(9):1261-1273. doi: 10.1093/jpp/rgac056.
MTH-3, a curcumin derivative, exhibits improved water solubility. This study aims to elucidate the mechanisms underlying the anticancer effects of MTH-3 on human oral squamous cell carcinoma CAL27 cisplatin-resistant (CAR) cells.
To evaluate the biological functions of MTH-3 in CAR cells, flow cytometry, staining, and western blot analyses were used.
MTH-3 reduced CAR cell viability and significantly induced autophagy in the presence of 10 and 20 μM MTH-3. Transcription factor EB was identified as the potential target of MTH-3. Autophagy-related proteins were upregulated after 24 h of MTH-3 incubation. MTH-3 treatment increased caspase-3 and caspase-9 enzyme activities. Mitochondrial membrane potential was decreased after MTH-3 treatment. MTH-3 triggered the intrinsic apoptotic pathway.
MTH-3 induces autophagy and apoptosis of CAR cells via TFEB. MTH-3 might be an effective pharmacological agent for treating oral cancer cells.
姜黄素衍生物 MTH-3 具有改善的水溶性。本研究旨在阐明 MTH-3 对人口腔鳞状细胞癌 CAL27 顺铂耐药（CAR）细胞的抗癌作用的机制。
为了评估 MTH-3 在 CAR 细胞中的生物学功能，使用流式细胞术、染色和 Western blot 分析。
在存在 10 和 20 μM MTH-3 的情况下，MTH-3 降低了 CAR 细胞活力并显著诱导自噬。转录因子 EB 被鉴定为 MTH-3 的潜在靶标。自噬相关蛋白在 MTH-3 孵育 24 小时后上调。MTH-3 处理增加了 caspase-3 和 caspase-9 酶的活性。线粒体膜电位在 MTH-3 处理后降低。MTH-3 触发了内在的凋亡途径。
MTH-3 通过 TFEB 诱导 CAR 细胞的自噬和凋亡。MTH-3 可能是治疗口腔癌细胞的有效药物。
