## 1 Introduction  
Cancer is a hyperproliferative disease controlled by multiple genes and various cell signaling pathways. In the past, cancer treatment mainly involved the use of high doses of systemic and non-specific chemotherapy drugs [1]. Unfortunately, severe non-selective toxicity and the development of resistance have limited the use of many drugs [2]. Therefore, the pharmacological approaches to this difficult pathology increasingly require targeted and precise strategies [3, 4]. The advanced technology and a better understanding of the genetic cancer cell changes have facilitated the development of a new generation of targeted anticancer treatments [5]. Recently, the use of natural compounds as anticancer agents is rapidly gaining popularity [6] because of their effectiveness against different types of cancer and inducing negligible or no toxic effects [7]. Amongst them, RSV is a natural stilbene with interesting antioxidant, anti-inflammatory, cardioprotective, and anticancer properties [8]. RSV can switch multi-resistance in cancer cells, and it is also able to make cancer cells more sensitive to chemotherapeutic compounds when used in combination with traditional anticancer drugs [9]. Numerous novel analogs of RSV have been prepared with augmented anticancer activity, bioavailability, and pharmacological profile [10; 11; 12; 13; 14]. In our previous work [10], we described the anticancer activity of a series of synthetic RSV phenylacetamide analogs, synthetized by some of us [15]. These compounds possess a monosubstituted aromatic ring that mimics the RSV phenolic nucleus and a longer flexible chain that makes them more stable than RSV. Among the studied compounds, the derivative **2** (Figure 1) resulted in being more bioavailable than RSV and was the most active in exerting anti-inflammatory and anti-proliferative effects, without showing cytotoxicity on healthy cells. In particular, this compound triggered cell cycle arrest and apoptosis in the estrogenic receptor-positive (ER+) MCF-7 and triple-negative MDA-MB-231 breast cancer cells.  
Accumulating evidence demonstrates that RSV can interfere with the invasion and migration processes in different tumors via numerous mechanisms and signaling pathways [16]. Thus, in this work, we studied the ability of the most active RSV phenylacetamide (derivative **2**) to interfere with the migration and metastatic processes. During the epithelial-mesenchymal transition (EMT), cancer cells gain migratory and invasive properties that involve a dramatic reorganization of the cytoskeleton components [17]. First, we performed docking studies of derivative **2** on two cytoskeleton major targets, namely tubulin and actin. The obtained results demonstrate that the derivative **2** binds both proteins with high energy and affinity. Then, using immunofluorescence and specific in vitro assays, we confirmed that the derivative **2** effectively acts as a tubulin and actin polymerization inhibitor. In addition, it is also able to accelerate the actin depolymerization, similarly to Latrunculin A, a toxin that causes a rapid disassembly of actin filaments and favors the depolymerization process [18]. Furthermore, the derivative **2** interferes with the metastatic and migratory potential in both the breast cancer MCF-7 and MDA-MB-231 in vitro. Taken together, the obtained results demonstrated that the derivative **2** could represent an interesting new agent useful for the development of safe and effective anticancer drugs targeting cytoskeleton dynamics and blocking the metastatic potential in breast cancer.