Fig. 7: Hypoxia-mediated tumor phenotypes can be overcome by NONO knockout.
A, B Extracellular acidification rate (ECAR) of HepG2 (A) and SMMC-7721 (B) cells with NONO knockout or not were determined by Seahorse XF assays after treating with Cocl2 (100 μM) for 24 h or not. C In vitro tube formation assays incubated with condition medium from indicated cells. The number of branch points quantified by image J. D The cell viability HepG2 cells with NONO knockout or not under hypoxia or normoxia was determined by colony formation assay. E The wound-healing assay in SMMC-7721 cell with NONO-KO or not was determined after hypoxia or normoxia treatment. The area of wound healed was measured by image J. F The wound-healing assay in Huh7 cell with NONO-overexpressing or not was determined after hypoxia or normoxia treatment. The area of wound healed was measured by image J. G HepG2 cells with NONO knockout or not were treated with sorafenib at indicated concentration for 48 h in the presence or absence of oxygen, then the cell viability was determined by CCK-8 assay. H Enhanced response to sorafenib due to NONO knockdown was observed in sorafenib-resistant Hep3B (left) and Huh7 (right). The IC50 of each treatment is presented. I The volume and weight of subcutaneous tumors in different treatment groups was determined (n = 10). J Mice bearing tumors xenografts were treated as described in “Materials and Methods”. Curves of tumor growth in each group were measured.
