Autophagy is a process by which lysosomes degrade and recycle long‐lived proteins and cellular organelles. It degrades cellular components that are worn out/damaged or needed to generate substrates to maintain cellular energy homeostasis under conditions of limited nutrients or stress. Cells of squamous cell cancer of the head and neck (HNSCC), which is the fifth most common malignancy in the world, have a high expression of the SET protein and under oxidative stress they perform the autophagic process. Therefore, the aim of our study is to verify a potential involvement of the SET protein on the autophagic process in these cells exposed to oxidative stress. Initially, knockdown of the SET protein (siSET) was performed in the Cal 27 cell line, in which oxidative stress was induced with tert‐butylhydroperoxide (t‐BHP). Proteins involved in autophagy as LC3B, Beclin‐1 and p62 were analyzed by immunoblotting. The siSET in Cal 27 cells caused an increase in the level of these proteins, which was slightly and significantly reduced after 4 and 8 hours of exposure to t‐BHP, respectively. Acids vacuoles identified by immunofluorescence, which are indicative of autophagy, were also found in Cal 27 cells for siSET and treatment with t‐BHP. Therefore, we believed that SET protein is important for the modulation of autophagy in HNSCC. PCR array assays are now in progress in order to assess potential genes involved in this regulation.FAPESP and CAPES
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