TTN-AS1 accelerates the growth and migration of nasopharyngeal carcinoma cells via targeting miR-876-5p/NETO2

Nasopharyngeal carcinoma (NPC) is one of the most predom-inant cancers occurring in China with high morbidity. Lately, large quantities of long non-coding RNAs (lncRNAs) have been highlighted to regulate the biological activities in multi-ple tumors, including NPC. Our study centered on whether TTN-AS1 was involved in NPC and how it modulated the pro-gression of NPC. Here, qRT-PCR data uncovered that TTN-AS1 expression was conspicuously high in NPC cells. Based on the results of functional assays, TTN-AS1 silence hampered the proliferative, migratory, and invasive abilities but stimu-lated the apoptotic capability of NPC cells. After a series of mechanism assays, TTN-AS1 was found to competitively bind with miR-876-5p and recruit UPF1 to enhance NETO2 expression. In addition, TTN-AS1 could be transcriptionally activated by YY1 in NPC cells. It was also found that miR-876-5p overexpression or NETO2 downregulation had inhibi-tory effects on cell proliferation, migration, and invasion in NPC. Moreover, NETO2 upregulation could restore the sup-pressive impacts of TTN-AS1 depletion on NPC cell and tumor growth. In conclusion, YY1-activated TTN-AS1 inter-acted with both miR-876-5p and UPF1 to upregulate NETO2, thus strengthening NPC cell malignant behaviors, which might provide more useful information for people to develop effective NPC treatments.

Automated summary

This study focused on the involvement of TTN-AS1 in nasopharyngeal carcinoma (NPC) and its impact on the progression of NPC. The results showed that TTN-AS1 was highly expressed in NPC cells and its depletion inhibited cell proliferation, migration, and invasion while stimulating apoptosis. TTN-AS1 was found to interact with miR-876-5p and UPF1, enhancing the expression of NETO2. Additionally, TTN-AS1 could be transcriptionally activated by YY1 in NPC cells. These findings provide valuable insights into the development of effective treatments for NPC.