MiR‐9‐1 targets HK2 and negatively modulates glycolysis metabolism in nasopharyngeal carcinoma (NPC) cells. A, The relative expression of HK2 (hexokinase 2), MTHFD2 (encoding methylenetetrahydrofolate dehydrogenase [NADP+dependent] 2), and MTHFD1L (encoding methylenetetrahydrofolate dehydrogenase [NADP+dependent] 1 like) in NPC cell lines. B, The protein abundance of HK2 in normal nasopharyngeal NP69 cells and NPC cell lines was detected using Western blotting. C, MicroRNA (miRNA) luciferase reporter assays of SUNE1 and HNE1 cells transfected with a wild‐type or mutated HK2 reporter plus negative control (NC), miR‐9‐1 mimics, anti‐NC, or anti‐miR‐9‐1, respectively. D, Western blotting analysis indicated that HK2 levels were decreased in SUNE1 and HNE1 cells transfected with miR‐9‐1 mimics, but increased in those transfected with the miR‐9‐1 inhibitor; α‐tubulin was used as the loading control. E, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assays in SUNE1 and HNE1 cells transfected with miR‐9‐1 mimics plus empty vector or miR‐9‐1 mimics plus the HK2 expression vector, compared with the negative control group. F, Transfection of miR‐9‐1 mimics inhibited the plate clone formation capabilities in SUNE1 and HNE1 cells; HK2 could reverse the ability of colony formation. **P < .01, ***P < .001