P32 | BLOCKING CANCER CELL MOVEMENT: THE ROLE OF PAXILLIN AND EZRIN IN CERVICAL TUMOR

M. Hałas-Wiśniewska¹, W. Arendt¹, M. Gagat^1,2, M. Izdebska¹ | ¹Department of Histology and Embryology, Nicolaus Copernicus University in Toruń, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Poland; ²Faculty of Medicine, Collegium Medicum, Mazovian Academy in Płock, Poland

Cervical cancer remains one of the most common malignancies affecting women worldwide, with metastasis being a key factor contributing to poor prognosis and treatment failure. Understanding the molecular mechanisms underlying cancer cell migration and invasion is essential for identifying new therapeutic targets. In this context, cytoskeleton-associated proteins such as paxillin (PXN) and ezrin (EZR) have gained increasing attention due to their role in linking actin microfilaments to the cellular environment and modulating cell motility. This study aimed to investigate the influence of PXN and EZR on the metastatic potential of cervical cancer cells. Using two cell lines -SiHa (derived from a primary cervical lesion) and HT-3 (from lymph node metastasis)- we examined how silencing the expression of these proteins affects key cellular processes. siRNA was employed to reduce PXN and EZR levels, followed by assays to evaluate changes in adhesion, migration, invasion, and response to cisplatin, a commonly used chemotherapeutic agent. The results demonstrated that reduced expression of both PXN and EZR significantly impairs the adhesive and migratory capabilities of cervical cancer cells. Notably, disruption of EZR expression led to a pronounced reorganization of the actin cytoskeleton and the appearance of cells with a mitotic catastrophe-like phenotype. Furthermore, knockdown of either protein enhanced cellular sensitivity to cisplatin, suggesting an additional benefit in the context of chemotherapy. In conclusion, PXN and EZR play a crucial role in regulating cervical cancer cells’ invasive and metastatic potential. Their inhibition limits cell motility and increases susceptibility to cytotoxic treatment. These findings support the potential of PXN and EZR as targets for novel anti-metastatic strategies in cervical cancer therapy.