Thus, it is important to comprehend the action of these drugs at different concentrations in different systems to confirm its preferential activity against a target cell type. Drugs that cause DNA breakage commonly result in cell cycle arrest and the activation of apoptosis [40]. Several of

these drugs cause nuclear alterations by disruption of cytoskeletal organization. Microtubule disruption could also cause G2/M arrest prior to inducing cell death by apoptosis [45, 46]. Thus, we investigated the cytoskeletal patterns of cells that were treated with cinnamic acid. The control group showed a microtubule Selleckchem 4EGI-1 network that was very finely departed from the centrosome region near the nucleus. A visible disorganization of the tubulin filaments was detected in interphasic treated cells. Cells treated with 3.2 mM cinnamic acid showed diffuse cytoplasmic staining and protein accumulation around the nucleus. Cells treated with a 0.4 mM dose of the drug did not demonstrate www.selleckchem.com/products/dinaciclib-sch727965.html alterations in the organization of their microtubule cytoskeleton.

Cytoplasmic retraction [47, 48] is a characteristic of apoptosis, and cytoskeletal disorders have been implicated in this Ilomastat cost process [49]. Actin cleavage has been associated with many characteristics of pre-apoptotic cells [50], and microfilament reorganization is essential to apoptotic body formation in later stages of cell death [47]. The morphological changes observed in these cells revealed an association with actin filament depolymerization. Similar

effects were shown in studies conducted by Boggio et al. [51], which demonstrated that human fibroblasts from keloids treated with verapamil, a calcium antagonist, showed an altered bipolar to spherical morphology. Boggio et al. [51] showed disassembly of the actin network with the formation of shorter stress fibers in fibroblasts treated with verapamil. This was strongly associated with a change in cell morphology. The treatment of cells using anti-mitotic agents, such as taxol and taxotere, which maintain tubulin polymerization, revealed interesting alterations in the actin cytoskeleton. In these studies, MCF7 cells were treated Selleckchem Sorafenib with taxol or taxotere at concentrations of 10 μM or higher, which resulted in a decrease in peripheral microfilaments and progressive cytoplasmic actin accumulation and actin rings around the nuclei [52]. We demonstrated that the effects of cinnamic acid on the actin cytoskeleton in our model system were similar to those observed in other systems using different drugs. Cells treated with 3.2 mM cinnamic acid showed a sharp reduction in peripheral microfilaments, which was in contrast with many strongly stained clusters of F-actin located around the nuclei. Cytoskeletal damage is a characteristic of pre-apoptotic cells [50]. Mills et al.