Аннотация:Inactivation of normal p53 function by exogenous mutant forms with known dominant-negative effect, as well as the TP53 repression in A549 cells led to increased migration and invasion, proliferation, the growth rate of subcutaneous xenografts as well as increased metastasis of intrapulmonary A549 xenografts in nude mice. Exogenous TP53 WT expression in p53-negative cells H1299, on the contrary, suppressed proliferation and migration, significantly reduced orthotopic tumorigenicity and metastasis. The change in cell motility was associated with actin cytoskeleton reorganisation and shift in the actin isoforms ratio. Apparently, the shift in the ratio towards γ-actin predominance occurred as a result of ERK1/2 activation in cells with p53 dysfunction and led to enhanced neoplastic cell malignant properties.Conclusion Actin cytoskeleton reorganisation via increasing γ-actin level stimulated tumour progression and metastasis as a result of tumour suppressor p53 dysfunction and activation of MAPKs so γ-actin predominance could be a universal characteristic of neoplastic cells.