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.