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The translationally controlled tumor protein (TCTP) plays a role in cell growth, cell cycle and cancer&lt;br /&gt;progression. TCTP controls negatively the stability of the p53 tumor suppressor protein and interacts with the&lt;br /&gt;cellular cytoskeleton. The deregulation of the actin and cytokeratin cytoskeleton is responsible for the increased&lt;br /&gt;migratory activity of tumor cells and is linked with poor patient outcome. Recent studies indicate that cyclin A,&lt;br /&gt;a key regulator of cell cycle, controls actin organization and negatively regulates cell motility via regulation of RhoA&lt;br /&gt;expression. We studied the organization of actin and cytokeratin cytoskeleton and the expression of TCTP, p53,&lt;br /&gt;cyclin A, RhoA and actin in HIO180 non-transformed ovarian epithelial cells, and OVCAR3 and SKOV3 (expressing&lt;br /&gt;low level of inducible p53) ovarian epithelial cancer cells with different metastatic potential. Immunostaining&lt;br /&gt;and ultrastructural analyses illustrated a dramatic difference in the organization of the cytokeratin and actin&lt;br /&gt;filaments in non-transformed versus cancer cell lines. We also determined that there is an inverse relationship between&lt;br /&gt;the level of TCTP/RhoA and actin/p53/cyclin A expression in ovarian cancer cell lines. This previously unidentified&lt;br /&gt;negative relationship between TCTP/RhoA and actin/p53/cyclin A may suggest that this interaction is linked&lt;br /&gt;with the high aggressiveness of ovarian cancers.<br>The translationally controlled tumor protein (TCTP) plays a role in cell growth, cell cycle and cancer&lt;br /&gt;progression. TCTP controls negatively the stability of the p53 tumor suppressor protein and interacts with the&lt;br /&gt;cellular cytoskeleton. The deregulation of the actin and cytokeratin cytoskeleton is responsible for the increased&lt;br /&gt;migratory activity of tumor cells and is linked with poor patient outcome. Recent studies indicate that cyclin A,&lt;br /&gt;a key regulator of cell cycle, controls actin organization and negatively regulates cell motility via regulation of RhoA&lt;br /&gt;expression. We studied the organization of actin and cytokeratin cytoskeleton and the expression of TCTP, p53,&lt;br /&gt;cyclin A, RhoA and actin in HIO180 non-transformed ovarian epithelial cells, and OVCAR3 and SKOV3 (expressing&lt;br /&gt;low level of inducible p53) ovarian epithelial cancer cells with different metastatic potential. Immunostaining&lt;br /&gt;and ultrastructural analyses illustrated a dramatic difference in the organization of the cytokeratin and actin&lt;br /&gt;filaments in non-transformed versus cancer cell lines. We also determined that there is an inverse relationship between&lt;br /&gt;the level of TCTP/RhoA and actin/p53/cyclin A expression in ovarian cancer cell lines. This previously unidentified&lt;br /&gt;negative relationship between TCTP/RhoA and actin/p53/cyclin A may suggest that this interaction is linked&lt;br /&gt;with the high aggressiveness of ovarian cancers.