Serine Threonine Tyrosine Kinase 1 (STYK1) presents oncogenic properties in many studies, and emerging evidence suggests that ferroptosis serve as a novel tumor suppressor. However, the interplay between STYK1 and ferroptosis in NSCLC remains unclear. Our aim is to illustrate the expression of ferroptotic regulator Glutathione peroxidase 4 (GPX4) in NSCLC and the relationship between STYK1 and ferroptosis. Herein, results based on ONCOMINE database, clinical specimens, and cellular manipulation revealed GPX4 was upregulated in NSCLC tissues and cell lines, and high GPX4 expression predicted worse prognosis. High STYK1 expression predicted worse OS and was related to high GPX4 in NSCLC tissues; overexpression of STYK1 in lung cancer cell line SW900 upregulated the expression of GPX4, promoted proliferation, and attenuated diverse mitochondrial abnormalities specific to ferroptosis, whereas knockdown of GPX4 exacerbated such attenuations without affecting cell proliferation. Taken together, ferroptosis as an anti-tumor factor is inhibited in NSCLC, and targeting ferroptosis could be a novel therapeutic strategy for the management of NSCLC; furthermore, regulating ferroptosis could be another cancerous mechanism of STYK1.
Keywords: Ferroptosis; Glutathione peroxidase 4; NSCLC; Serine threonine tyrosine kinase 1.
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