Cancers, Vol. 12, Pages 3269: TSPAN1: A Novel Protein Involved in Head and Neck Squamous Cell Carcinoma Chemoresistance

Alexandros G.Sfakianakis shared this article with you from Inoreader Cancers, Vol. 12, Pages 3269: TSPAN1: A Novel Protein Involved in Head and Neck Squamous Cell Carcinoma Chemoresistance Μέσω Cancers Cancers, Vol. 12, Pages 3269: TSPAN1: A Novel Protein Involved in Head and Neck Squamous Cell Carcinoma Chemoresistance Cancers doi: 10.3390/cancers12113269 Authors: Yoelsis Garcia-Mayea Cristina Mir Laia Carballo Josep Castellvi Jordi Temprana-Salvador Juan Lorente Sergi Benavente Juana M. García-Pedrero Eva Allonca Juan P. Rodrigo Matilde E. LLeonart Sensitization of resistant cells and cancer stem cells (CSCs) represents a major challenge in cancer therapy. A proteomic study revealed tetraspanin-1 (TSPAN1) as a protein involved in acquisition of cisplatin (CDDP) resistance (Data are available via ProteomeXchange with identifier PXD020159). TSPAN1 was found to increase in CDDP-resistant cells, CSCs and biopsies from head and neck squamous cell carcinoma (HNSCC) patients. TSPAN1 depletion in parental and CDDP-resistant HNSCC cells reduced cell proliferation, induced apoptosis, decreased autophagy, sensitized to chemotherapeutic agents and inhibited several signaling cascades, with phospho-SRC inhibition being a major common target. Moreover, TSPAN1 depletion in vivo decreased the size and proliferation of parental and CDDP-resistant tumors and reduced metastatic spreading. Notably, CDDP-resistant tumors showed epithelial–mesenchymal transition (EMT) features that disappeared upon TSPAN1 inhibition, suggesting a link of TSPAN1 with EMT and metastasis. Immunohistochemical analysis of HNSCC specimens further revealed that TSPAN1 expression was correlated with phospho-SRC (pSRC), and inversely with E-cadherin, thus reinforcing TSPAN1 association with EMT. Overall, TSPAN1 emerges as a novel oncogenic protein and a promising target for HNSCC therapy. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.