Malignant cell transformation requires changes in the ability of cells to migrate. The disruption of actin cytoskeleton and intercellular adhesions is an important component of the acquisition of invasive properties in epithelial
malignancies. The invasive ability of
carcinoma cells is associated with reduced expression of adhesion junction molecules and increased expression of mesenchymal markers, frequently referred to as epithelial-to-mesenchymal transition (EMT). Standard features of the EMT program in
cancer cells include fibroblastic phenotype, downregulation of the epithelial marker
E-cadherin, induction of
Snail-family transcription factors, as well as expression of mesenchymal
proteins. We compared the epithelial and mesenchymal marker profiles of nonmalignant HaCaT keratinocytes to the corresponding profiles of cervical
carcinoma cell lines C-33A, SiHa, and CaSki. The characteristics of the EMT appeared to be more developed in SiHa and CaSki
cervical cancer cells. Further activation of the EMT program in
cancer cells was induced by
epidermal growth factor. Decreased epithelial marker
E-cadherin in CaSki cells was accompanied by increased mesenchymal markers
N-cadherin and
vimentin. Downregulated expression of
E-cadherin in SiHa and CaSki cells was associated with increased expression of Snail
transcription factor. Our goal was to study actin reorganization in the EMT process in cell cultures and in tissue. We found that β-cytoplasmic actin structures are disorganized in the
cervical cancer cells. The expression of β-cytoplasmic actin was downregulated.