CD73 and cN-II regulate the cellular response to chemotherapeutic and hypoxic stress in lung adenocarcinoma cells

Cytosolic 5′-nucleotidase II (cN-II) and ecto-5′-nucleotidase (CD73) are enzymes involved in the nucleotide metabolism by dephosphorylating nucleoside monophosphates. Both cancer modifying anticancer drug activity, cell biology immune modulation. We have modified lung cells (NCI-H292) to become deficient for either or both using CRISPR/Cas9 technique, studied implication of two cellular response different stress condition i.e. chemotherapeutic agents, hypoxia stress. Our results show that there is no significant role these proliferation under hypoxic Similarly, cN-II CD73 not wound healing ability CoCl2-mediated HIF-1α stabilization. Furthermore, our CD73-deficiency associated with increased apoptosis 1600 μM adenosine, decreased sensitivity mitomycin enhanced vincristine. deficiency vivo tumor growth vincristine C. study gives new insights into biological roles conditions this particular line. Further experiments will help deciphering molecular mechanisms underlying observed differences.