We then treated these cell lines with 5-aza-2-deoxycytidine (5-AZA) and/or Trichostatin A (TSA) and found that LINC00152 expression was increased by 16-fold in H526 and 8-fold in H146 cells after TSA treatment, whereas, 5-AZA didn’t change LINC00152 expression (Fig. 3C), indicating that histone acetylation could be one mechanism causing LINC00152 overexpression in NSCLC. Here, CYTOR is linked to non-small cell lung carcinoma.