Long non-coding RNA TP73-AS1 accelerates the progression and cisplatin resistance of non-small cell lung cancer by upregulating the expression of TRIM29 via competitively targeting microRNA-34a-5p

Non-small cell lung cancer (NSCLC) is a leading subtype of lung cancer, with high mortality rates. Recently, long non-coding RNAs (lncRNAs) have been associated with NSCLC. The present study aimed to examine the role of the TP73 antisense RNA 1 (TP73-AS1) lncRNA in NSCLC. TP73-AS1 and microRNA(miR)-34a-5p expression levels were measured using reverse transcription-quantitative PCR (RT-qPCR) and chromogenic in situ hybridization (CISH). Cell proliferation, apoptosis, migration and invasion was determined using Cell Counting Kit-8 (CCK-8), flow cytometry, Transwell and Matrigel assays, respectively. The median inhibitory concentration (IC(50)) value of cisplatin (cis-diamminedichloroplatinum; DDP) was assessed using a CCK-8 assay. The interaction between miR-34a-5p and TP73-AS1 or tripartite motif-containing 29 (TRIM29) was predicted using microRNA.org and Starbase, then verified using a dual-luciferase reporter assay. The expression of TRIM29 was quantified at the mRNA and protein level using RT-qPCR and western blot analysis, respectively. TP73-AS1 was significantly upregulated, while miR-34a-5p was downregulated in NSCLC tissues and cells. Functionally, TP73-AS1 knockdown inhibited proliferation, migration, invasion and DDP resistance, whilst inducing apoptosis in NSCLC cells. miR-34a-5p was identified as a target for TP73-AS1, and its inhibition reversed the effects of TP73-AS1 knockdown on NSCLC cells. In addition, TRIM29 was targeted by miR-34a-5p, and its overexpression reversed the effects of miR-34a-5p. Moreover, TP73-AS1 acted as a molecular sponge for miR-34a-5p, increasing the expression of TRIM29. In conclusion, TP73-AS1 contributed to proliferation, migration and DDP resistance but inhibited apoptosis of NSCLC cells by upregulating TRIM29 and sponging miR-34a-5p.