| Literature DB >> 30017201 |
Toshifumi Fujiwara1, Takanori Eguchi2, Chiharu Sogawa3, Kisho Ono4, Jun Murakami5, Soichiro Ibaragi6, Jun-Ichi Asaumi7, Kuniaki Okamoto3, Stuart K Calderwood8, Ken-Ichi Kozaki3.
Abstract
Genetic amplification, overexpression, and increased signaling from the epidermal growth factor receptor (EGFR) are often found in oral squamous cell carcinoma (OSCC) and thus EGFR is frequently targeted molecularly by the therapeutic antibody cetuximab. We assessed effects of cetuximab in control of EGF-driven malignant traits of OSCC cells. EGF stimulation promoted progression level of mesenchymal traits in OSCC cells, which were attenuated by cetuximab but incompletely. We pursued a potential mechanism underlying such incomplete attenuation of OSCC malignant traits. Cetuximab promoted secretion of EGFR-EVs by OSCC cells and failed to inhibit EGF-driven secretion of EGFR-EVs. Cetuximab was also found to be robustly secreted with the EGFR-EVs by the OSCC cells. Thus, EGF promotes the level of mesenchymal traits of OSCC cells and secretion of EGFR-EVs, which involve cetuximab resistance.Entities:
Keywords: Anti-EGFR antibody therapy; Cetuximab; Epithelial-to-mesenchymal transition; Extracellular vesicles; Head and neck squamous cell carcinoma
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Year: 2018 PMID： 30017201 DOI： 10.1016/j.bbrc.2018.07.035
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575