Abstract This study aimed to evaluate the synergistic anticancer effect of vinblastine and WYE-132, a specific inhibitor of the mammalian target of rapamycin (mTOR), on B16F10 melanoma cancer cells. MTT assay, Annexin V, and DAPI staining along with Real-Time PCR were conducted to understand the mechanistic roles of mTOR pathway in melanoma cancer cells. The IC50 values for vinblastine and WYE-132 were 39.4 ± 1.8 nM and 145.2 ± 4.5 nM, respectively. The co-administration of WYE-132 and vinblastine in B16F10 cells offered a significant increase in the growth inhibitory effect of vinblastine along with a two-fold escalation in the percentage of apoptotic cells. The calculation of gene expression levels confirmed a visible fall in anti-apoptotic Bcl-2, Ki-67 and Mcl-1 accompanied by a surge in pro-apoptotic Bax mRNA levels (p

中文翻译：

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利用 WYE-132 作为 mTOR 信号的抑制剂增强长春碱对 B16F10 黑色素瘤癌细胞的细胞毒性作用

摘要 本研究旨在评估长春碱和 WYE-132（一种哺乳动物雷帕霉素靶蛋白 (mTOR) 的特异性抑制剂）对 B16F10 黑色素瘤癌细胞的协同抗癌作用。进行 MTT 测定、膜联蛋白 V 和 DAPI 染色以及实时 PCR，以了解 mTOR 通路在黑色素瘤癌细胞中的机制作用。长春碱和 WYE-132 的 IC50 值分别为 39.4 ± 1.8 nM 和 145.2 ± 4.5 nM。WYE-132 和长春碱在 B16F10 细胞中的共同给药显着增加了长春碱的生长抑制作用，同时凋亡细胞的百分比增加了两倍。基因表达水平的计算证实了抗凋亡 Bcl-2、Ki-67 和 Mcl-1 的明显下降，伴随着促凋亡 Bax mRNA 水平的激增（p