Focal Adhesion and Cancer Cell Cycle-Associated Resistance

The mechanisms underlying cancer cell drug resistance have not yet been fully elucidated. Numerous processes hinder effective tumor treatment, such as cancer cell epigenetic alterations, DNA repair, drug target modification, and epithelial-mesenchymal transition. Recent studies have highlighted the ability of cancer cells to transiently enter the resting phase, namely, the G0 phase of the cell cycle under treatment conditions; this is associated with an elevated level of cell death. Cells in the G0 phase are characterized by a specific phenotype, the exact features of which remain to be fully elucidated. Cell division and cell cycle dynamics are closely associated with cell adhesion, i.e., interaction with the extracellular matrix in normal cells, whereas cancer cells are characterized by the dys-coordination of these processes. However, the precise patterns of cell adhesion alterations in association with the cell cycle remain unclear. Knowledge on the interactions of cells in the G0 phase with the extracellular matrix during the entry, the exit, and the sustenance during the resting phase is limited. At the same time, focal adhesion-mediated molecules may be an attractive goal for cancer cells in the G0 phase, targeting to overcome tumor dissemination and drug resistance. Drug resistance and immune system response evasion are specific features of nonproliferating cancer cells that call for more detailed and accurate characterization of this population of malignant cells to optimize anticancer treatment and control tumor dissemination. The present review represents the recent data on the association of focal adhesion and cancer cell surveillance due to cell cycle alterations.