LINC01116 accelerates nasopharyngeal carcinoma progression based on its enhancement on MYC transcription activity

Long noncoding RNAs (lncRNAs) have been demonstrated to be frequently involved in the development of cancers, whereas only a few of them was investigated in nasopharyngeal carcinoma (NPC). Here, we found that LINC01116 was highly expressed in NPC cell lines, and inhibition of LINC01116 notably restrained cell viability, proliferation, and migration in NPC cells. Besides, we unveiled that LINC01116 was mainly distributed in the cytoplasm of NPC cells. Surprisingly, the cytoplasmic LINC01116 could directly interact with the 5′UTR of MYC mRNA, whereas such interaction had no influence on MYC mRNA expression, but facilitated MYC mRNA translation so as to enhance MYC protein level in NPC cells. Moreover, LINC01116 per se had no impact on the transcription of MYC targets but affected their expression through MYC‐dependent manner. Furthermore, MYC overexpression offset the suppression of LINC01116 silence on NPC development. In turn, we discovered that MYC could also serve as the transcriptional activator of LINC01116 in NPC cells. By and large, our findings elucidated a LINC01116/MYC feedback loop in accelerating the tumorigenesis of NPC, revealing a promising target to establish novel biomarkers for NPC patients. LINC01116 contributes to cell proliferation and migration in nasopharyngeal carcinoma. Cytoplasmic LINC01116 interacts with MYC mRNA to stimulate MYC protein and therefore enhance MYC transcriptional activity in nasopharyngeal carcinoma cells. LINC01116 is transactivated by MYC protein in turn. The contribution of LINC01116 to nasopharyngeal carcinoma progression is mediated by MYC.