Sabatini Maria Elisa, Compagnoni Micaela, Maffini Fausto, Miccolo Claudia, Pagni Fabio, Lombardi Mariano, Brambilla Virginia, Lepanto Daniela, Tagliabue Marta, Ansarin Mohssen, Citro Simona, Chiocca Susanna
Department of Experimental Oncology, IEO, European Institute of Oncology IRCCS, IEO Campus, Milan, Italy.
Division of Pathology, IEO, European Institute of Oncology, IRCCS, Milan, Italy.
Front Mol Biosci. 2022 Aug 12;9:940449. doi: 10.3389/fmolb.2022.940449. eCollection 2022.
Functional loss of E-cadherin is frequent during tumor progression and occurs through a variety of mechanisms, including proteolytic cleavage. E-cadherin downregulation leads to the conversion of a more malignant phenotype promoting Epithelial to Mesenchymal Transition (EMT). The UBC9/SUMO pathway has been also shown to be involved in the regulation of EMT in different cancers. Here we found an increased expression of UBC9 in the progression of Head and Neck Cancer (HNC) and uncovered a role for UBC9/SUMO in hampering the HPV-mediated E-cadherin cleavage in HNC.
E-钙黏蛋白的功能丧失在肿瘤进展过程中很常见,并且通过多种机制发生,包括蛋白水解切割。E-钙黏蛋白下调导致更具恶性表型的转变,促进上皮-间质转化(EMT)。UBC9/SUMO途径也已被证明参与不同癌症中EMT的调节。在这里,我们发现UBC9在头颈癌(HNC)进展中表达增加,并揭示了UBC9/SUMO在阻碍HNC中HPV介导的E-钙黏蛋白切割方面的作用。