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Prolyl hydroxylase 3 involvement in lung cancer progression under hypoxic conditions: association with hypoxia-inducible factor-1α and pyruvate kinase M2

   
@article{JTD31575,
	author = {Xiao Chu and Ming Xiang and Liang Feng and Hui Liu and Chao Zhou},
	title = {Prolyl hydroxylase 3 involvement in lung cancer progression under hypoxic conditions: association with hypoxia-inducible factor-1α and pyruvate kinase M2},
	journal = {Journal of Thoracic Disease},
	volume = {11},
	number = {9},
	year = {2019},
	keywords = {},
	abstract = {Background: Previous studies have suggested that the functions of prolyl hydroxylase 3 (PHD3) in tumor growth, apoptosis and angiogenesis are essentially dependent on hypoxia-inducible factor (HIF)-1α signaling. Nevertheless, whether PHD3 represents a promising tumor suppressor target remains to be clarified. To provide insight into the therapeutic potential of PHD3 in lung cancer, this study examined the effects of PHD3 expression on HIF-1α and pyruvate kinase M2 (PKM2), as well as on lung cancer cell proliferation, migration, and invasion.
Methods: The model of hypoxia was established in A549 and SK-MES-1 cells with 200 µM CoCl2 treatment, and verified by western blot and immunocytochemical staining. The expression levels of PKM2 and HIF-1α were determined by western blot after overexpression or depletion of PHD3 in A549 and SK-MES-1 cells. In addition, cell viability, migration and invasion were measured, respectively.
Results: Establishment of hypoxia in A549 and SK-MES-1 cells resulted in significant decreases in PHD3 expression and remarkable increase in PKM2 expression in 24 hrs. Overexpression of PHD3 in A549 and SK-MES-1 cells decreased HIF-1α and PKM2 expression. In contrast, PHD3 knockdown increased HIF-1α and PKM2 (P},
	issn = {2077-6624},	url = {https://jtd.amegroups.org/article/view/31575}
}