转化成简体中文并保留原句结构：导致转移性癌症如三阴性乳腺癌（TNBC）具有侵略性的基本机制是上皮-间充质转化（EMT）。在癌症微环境中，磷脂酰肌醇3-激酶（PI3K）-Akt-哺乳动物雷帕霉素靶蛋白（mTOR）信号通路在调控EMT机制方面起着关键作用。本研究重点研究雷帕霉素（一种新的针对mTOR的化疗药物）和MicroRNA（miR）-122对TNBC侵略行为的影响。使用MTT法确定4T1细胞的雷帕霉素半数抑制浓度（IC50）。此外，将miR-122暂时转染到4T1细胞中，以研究其对该通路的影响。采用定量实时聚合酶链反应（qRT-PCR）评估中央mTOR和EMT相关级联基因的表达水平。此外，使用刮痕和迁移实验评估细胞的运动和迁移。雷帕霉素和miR-122均显著降低PI3K、AKT和mTOR、ZeB1和Snail基因的表达水平。然而，Twist基因表达没有显著变化。此外，刮痕和迁移实验显示，4T1细胞的迁移明显减少，特别是在miR-122诱导后。我们的实验发现和基因富集研究表明，miR-122主要作用于多个代谢通路，以及EMT和mTOR，而雷帕霉素在癌细胞中的作用目标比较有限。因此，miR-122可以被认为是一种潜在的癌症微RNA治疗选项，其有效性可以在未来的动物研究中得到验证。

The fundamental mechanism responsible for the aggressiveness of metastatic cancers such as triple-negative breast cancer (TNBC) is the epithelial-mesenchymal transition (EMT). In cancer microenvironments, the Phosphoinositide 3-kinases (PI3K)-Akt- mammalian target of rapamycin (mTOR) signaling pathway plays a critical role in regulating the EMT mechanism. The current study focuses on the impacts of rapamycin, a newly retargeted chemotherapeutic agent against mTOR, and MicroRNA (miR)-122 on the aggressive behavior of TNBC.  The half-maximal inhibitory concentration (IC50) of rapamycin on 4T1 cells was determined using an MTT assay. Also, miR-122 was transiently transfected into 4T1 cells to study its effect on the pathway. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression level of central mTOR and EMT-related cascade genes. Moreover, cell mobility and migration were evaluated using scratch and migration assays, respectively. Both rapamycin and miR-122 significantly decreased the expression levels of PI3K, AKT, and mTOR, as well as ZeB1 and Snail genes. However, no significant change was observed in Twist gene expression. Furthermore, scratch and migration assays revealed that the migration of 4T1 cells was markedly reduced, especially following miR-122 induction. Our experimental findings and gene enrichment studies indicated that miR-122 mainly operates on multiple metabolic pathways, as well as EMT and mTOR, while rapamycin has restricted targets in cancer cells.  Consequently, miR-122 can be considered a potential cancer microRNA therapy option, which can be validated in the future in animal studies to demonstrate its efficacy in cancer control.