a Department of Biochemistry and Molecular Biology , Bengbu Medical College, Bengbu , Anhui , China.
b Research Center of Clinical Laboratory Science , Bengbu Medical College , Bengbu , Anhui , China.
Cell Cycle. 2017;16(24):2396-2403. doi: 10.1080/15384101.2017.1387699. Epub 2017 Nov 20.
Arsenic trioxide (ATO) has been reported to exert its anti-cancer activities in human cancers. However, the molecular mechanism of ATO-triggered anti-tumor activity has not been fully elucidated. Recently, multiple studies demonstrated that ATO could regulate miRNAs in human cancers. Therefore, in this study, we investigated whether ATO regulated let-7a in breast cancer cells. We found that ATO upregulated let-7a level in breast cancer cells. We also found that up-regulation of let-7a inhibited cell growth and induced apoptosis and retarded cell migration and invasion. We also observed that up-regulation of let-7a enhanced cell growth inhibition and invasion suppression induced by ATO treatment. Our findings suggest that ATO suppressed cell growth, stimulated apoptosis, and retarded cell invasion partly via upregulation of let-7a in breast cancer cells. Our study provides a new anti-tumor mechanism of ATO treatment in breast cancer.
三氧化二砷（ATO）已被报道在人类癌症中发挥抗癌作用。然而，ATO 触发抗肿瘤活性的分子机制尚未完全阐明。最近，多项研究表明 ATO 可以调节人类癌症中的 miRNAs。因此，在本研究中，我们研究了 ATO 是否调节乳腺癌细胞中的 let-7a。我们发现 ATO 上调了乳腺癌细胞中的 let-7a 水平。我们还发现，let-7a 的上调抑制了细胞生长并诱导了细胞凋亡，减缓了细胞迁移和侵袭。我们还观察到，let-7a 的上调增强了 ATO 处理诱导的细胞生长抑制和侵袭抑制。我们的研究结果表明，ATO 通过上调乳腺癌细胞中的 let-7a 抑制细胞生长、刺激细胞凋亡和减缓细胞侵袭。我们的研究为 ATO 治疗乳腺癌提供了一种新的抗肿瘤机制。
