The collective invasion effect of ezrin in lung cancer

In this project, the role of Ezrin in collective invasion was investigated in lung cancer, which is the most deadly cancer both worldwide and in our country. It has been determined that Ezrin exhibits oncogenic properties due to its impact on the spread of cancer cells and the transmission of signals from growth factors into the cell. Ezrin is a member of the ERM (Ezrin-Radixin-Moesin) family, which facilitates the connection between the cytoplasmic membrane and the cell's main protein, actin, forming the cell's cytoskeleton.Increased expression of Ezrin is associated with increased metastasis inhibition and survival time in non-small cell lung cancer. The process of primary cancer cells spreading to both regional and distant organs is complex. Studies in this field have shown that cancer cells can spread individually by undergoing epithelial-mesenchymal transition (EMT) or collectively as a group. In collective cell invasion, migrating cell clusters retain some of their unique epithelial characteristics and move as a whole unit in the areas they spread to. The purpose of this study is to determine the role of Ezrin expression in collective invasion of lung cancer cells. In this study, methods for establishing a collective invasion model in cell culture experiments were developed. A549 cells were silenced with Ezrin siRNA, and their collective migration in a wound healing assay was greatly suppressed, as shown by analysis using the ImageJ program. The suppression of Ezrin protein was demonstrated through the Western blot method. The relationship with Ezrin was elucidated by showing the mRNA expression levels of EMT genes through PCR analysis. Sections from paraffin tissue samples of NSCLC patients were analyzed immunohistochemically (IHC), revealing strong staining of Ezrin in collective invasion areas. Thus, it was demonstrated that Ezrin is important in NSCLC's collective invasion and that targeting Ezrin in lung cancer treatment could inhibit disease spread.