Center of Excellence for Molecular Imaging (CEMI), Department of Radiologic Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai 50200, Thailand.
Nanoscale. 2020 Mar 19;12(11):6556-6561. doi: 10.1039/c9nr10131d.
We herein report a new biological consequence from a unique interaction between nanoparticles of ferric-tannic complexes (Fe-TA NPs) and liver cancer cells (HepG2.2.15). The Fe-TA NPs were found to accumulate into the cells via specific cellular uptake mechanisms and thereafter disturbed cellular autophagy and cellular pH homeostasis, which led the cells to undergo autophagic stress and eventual death. According to biophysical analysis, the cells undergoing autophagic stress were found to lose their capability of attachment, migration, and movement. Similarly, KEGG analysis demonstrated the down-regulation of TGF-beta indicating that the autophagic stress is capable of reducing cancer cell invasion. Therefore, the Fe-TA NPs could be considered beneficial as a new pharmaceutical nanoplatform for liver cancer treatment via induction of autophagic stress.
我们在此报告了一种新的生物学后果，这是源于三价铁-鞣酸复合物（Fe-TA NPs）纳米颗粒与肝癌细胞（HepG2.2.15）之间的独特相互作用。研究发现，Fe-TA NPs 通过特定的细胞摄取机制进入细胞，然后干扰细胞自噬和细胞 pH 平衡，导致细胞发生自噬应激并最终死亡。根据生物物理分析，处于自噬应激状态的细胞丧失了附着、迁移和运动的能力。同样，KEGG 分析显示 TGF-β 的下调表明自噬应激能够降低癌细胞的侵袭能力。因此，Fe-TA NPs 可被视为通过诱导自噬应激而用于肝癌治疗的新型药物纳米平台。
