H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

LncRNAs can exhibit crucial roles in the development of multiple cancers, including non‐small cell lung cancer (NSCLC). Currently, we investigated the role of lncRNA H19 in NSCLC. In our study, it was found that H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS‐2B cells. Meanwhile, we observed that miR‐17 was downregulated in NSCLC cell lines. Inhibited H19 can suppress the growth, migration, and invasion of NSCLC cells and bioinformatics search was performed to predict the correlation between H19 and miR‐17. Overexpression of miR‐17 was able to inhibit the progression of NSCLC cells while reversely miR‐17 inhibitors reversed this process. In addition, signal transducers and activators of transcription (STAT3), as an mRNA target of miR‐17, was presented in our research. Moreover, we discovered that H19 demonstrated its biological functions via regulating miR‐17 and STAT3 in vitro. Silencing H19 greatly increased STAT3 expression by sponging miR‐19 in vitro. It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR‐17 in lung cancer. In summary, our findings indicated that H19/miR‐17/STAT3 axis participated in NSCLC development. H19 could be regarded as a significant prognostic biomarker in NSCLC progression. We showed that when H19 was silenced, the progression of NSCLC cells was significantly decreased by increasing miR‐17. A negative correlation between H19 and miR‐17 was suggested in our study, and STAT3 was targeted by miR‐17 in NSCLC progression. To conclude, our findings implied that H19 can be regarded as an oncogene in the promotion of NSCLC development and this is the first report on a novel mechanism for H19 in NSCLC.