Tai ultraviewer2/15/2023 Researches on entosis revealed that actomyosin contraction within the internalizing cells driven the formation of CIC structures 4, 5, which also requires intercellular adhesion mediated by adherens junction (AJ) 6. Homotypic CIC structures formation involves the invasion of one viable cell into another, which generally leads to the death of internalized cells in a non-apoptotic way that was termed Entosis 4. Thus, our work identifies CDKN2A as the first tumor suppressor whose inactivation promotes homotypic CIC formation in human cancer cells.Ī panel of human cancer tissues displayed unique cell-in-cell (CIC) structures 1, which were often associated with worse prognosis 2, 3. Moreover, CIC formation negatively correlates with p16INK4a expression in human breast cancers. The regulation of CIC formation by CDKN2A was tightly correlated with subcellular redistribution of E-cadherin, F-actin rearrangement and reduced phosphorylation of myosin light chain 2 (p-MLC2), consistent with which, CDKN2A expression imparted cells winner/outer identity in competition assay. We reported here that inhibiting CDKN2A expression effectively promoted homotypic CIC formation, whereas ectopic overexpression of p16INK4a or p14ARF, two proteins encoded by CDKN2A gene, significantly suppressed CIC formation in MCF7 cells. ![]() ![]() Although elevated CIC formation was found in cancers with CDKN2A inactivation, a causal link between them remains to be established. Cell-in-cell (CIC) structures, characterized by enclosure of one or more cells within another cell, were extensively documented in human cancers.
0 Comments
Leave a Reply.AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |