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DMFS in TNBC patients between high and low expression of cytoskeleton-associated genes on the Kaplan-Meier plotter database (K-O). It is well known that EMT and metastasis play an important role in the acquisition of the malignant phenotype of cancer cells (41).

We set out to explore whether lovastatin could inhibit breast CSCs by reversal of the EMT program and inhibition of metastasis in TNBC. Our study demonstrated that both the expression of mesenchymal markers such as Vimentin and EMT-related transcription factors such as Twist could be down-regulated by treatment with lovastatin in MDA-MB-231 CSCs.

Sensors and actuators b chemical present study also showed that lovastatin could inhibit liver metastasis as evidenced by reduced nodule formation and confirmed histopathologically by eliminated cancer cell colonization. In our animal model, we also examined the lungs for metastasis. One speculation is that the cells we used sensors and actuators b chemical CSCs, rather than bulk tumor cells, and the difference in signaling pathways between them may lead to the difference in metastatic spreading of tumor cells to different target organs.

These results provided solid evidence that lovastatin could inhibit the EMT program and metastasis in TNBC CSCs in vitro and in vivo.

In the process of EMT, tumor cells gain migratory and metastatic properties that involve a dramatic reorganization of the actin cytoskeleton and the concomitant formation of membrane protrusions required for invasive growth (41, 42). Emerging evidence suggests that cytoskeleton regulatory proteins are a convergent node of signaling pathways emanating from extracellular stimulus to cell movement. The coordinated activity of various cytoskeleton-binding proteins regulates a variety of cytoskeleton-based processes, including assembly of the microfilament and cell motility.

Actin cytoskeleton remodeling is an upstream regulator of EMT in metastatic breast cancer cells (43), and several studies clarified EMT was driven by actin cytoskeleton remodeling in hepatocellular and colorectal carcinoma (44, 45).

In our study, we demonstrated lovastatin induced rearrangement of the actin cytoskeleton favoring perinuclear and nuclear localization of F-actin filaments. Location of actin filaments underneath the plasma membrane is important for the formation of cellular protrusions such as lamellipodia and filopodia (48). Our results further showed that the number of pseudopodia of TNBC CSCs after lovastatin-treated were reduced, which confirmed cytoskeleton organization pathway play an important role in the lovastatin inhibition EMT and metastasis sensors and actuators b chemical TNBC CSCs.

We have demonstrated that lovastatin inhibited the EMT and metastasis of TNBC CSCs. This is supported by bioinformatics analysis showing that the cytoskeleton-associated genes are differentially expressed between TNBC lioresal non-TNBC tissues samples and that higher expression levels of these genes are associated with survival outcomes in TNBC patients.

In summary, our present study sensors and actuators b chemical provided evidence, for the first time, that lovastatin, a natural HMG-CoA fred inhibitor, inhibits TNBC CSCs in vitro and in vivo through inhibition of EMT phenotype and suppression of metastasis by dysregulation of cytoskeleton-associated proteins.

This study lays the foundation for the understanding of the inhibitory effect of lovastatin on the EMT and metastasis of TNBC CSCs sensors and actuators b chemical has potential clinical implications for the future management of TNBC. Further studies are required to move forward our effort toward resolving the issues of how lovastatin causes disturbance of the cytoskeleton organization pathway and how protein Ksucc contributes to lovastatin-induced EMT and sensors and actuators b chemical in TNBC CSCs.

Publicly available datasets were analyzed in this study. The animal study was reviewed and approved by Hunan Normal University Institutional Animal Care and Ethics Committee. CZ, SY, LL, Sensors and actuators b chemical, and GH performed the experiments.

SC, YL, XP, and ZC collected and analyzed the data. CZ, SY, and LL drafted the manuscript. MW, QZ, GL, and SF reviewed the manuscript. XD conceived and designed the research.

This work was supported by the National Natural Science Foundation of China (81872167, 81472496), Key Grant of Research and Development in Hunan Province (2020DK2002), Natural Science Foundation sensors and actuators b chemical Hunan (2019JJ40193), and Key Project of Department of Education of Hunan Province (14A089).

We thank Songqing Fan, Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China, and Jianmin Xi, Department of Pathology, Hunan Academy of Traditional Chinese Medicine Affiliated Hospital, Changsha, Hunan, China, for expert evaluation of metastatic tumor cells and quantitative analysis of the metastatic burden.

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