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
- Shunxiang Luo
- Ming Shen
- Hui Chen
- Weiwei Li
- Cong Chen
Affiliations: Department of Oncology, The First People's Hospital of Tianmen, Tianmen, Hubei 431700, P.R. China
- Published online on: September 1, 2020 https://doi.org/10.3892/mmr.2020.11473
Copyright: © Luo
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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 (IC50) 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.