{'fraction_non_alphanumeric': 0.030868167202572346, 'fraction_numerical': 0.02572347266881029, 'mean_word_length': 5.101960784313725, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
MicroRNA-370 inhibits the progression of non-small cell lung cancer by downregulating oncogene TRAF4.

Lung cancer is the leading cause of cancer-related deaths, of which most can be attributed to non-small cell lung cancer (NSCLC). microRNAs (miRNAs) are a group of small non-coding RNAs that focus on post-transcriptional modification. The present study aimed to investigate the role and function of microRNA-370 (miR-370) in NSCLC and explore the underlying functional mechanisms. We found that miR-370 was significantly downregulated in the tumor tissues of NSCLC patients as well as in NSCLC cell lines. Overexpression of miR-370 by infection of recombinant lentivirus markedly inhibited cell proliferation and promoted cell apoptosis of NSCLC cells. In addition, in vivo tumor formation of NSCLC cells was decreased by miR-370 overexpression. Through bioinformatic analysis, we found that tumor necrosis factor receptor-associated factor 4 (TRAF4), an oncogene as previously reported, was predicted as a putative target gene of miR-370. The direct targeting relationship between miR-370 and the 3'-untranslated region was validated by dual-luciferase reporter assay. Furthermore, overexpression of miR-370 downregulated the protein expression of TRAF4 in the NSCLC cells. Moreover, the growth inhibitory effect of miR-370 overexpression on NSCLC cells was abrogated by TRAF4 overexpression. In conclusion, our results suggest that miR-370 plays an important role in NSCLC by regulating TRAF4 and may be a potential target for the treatment of NSCLC.