Dataset Information

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.

ABSTRACT: 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.

SUBMITTER: Luo S

PROVIDER: S-EPMC7533438 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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.

Luo Shunxiang S Shen Ming M Chen Hui H Li Weiwei W Chen Cong C

Molecular medicine reports 20200901 5

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 de ...[more]

PMID: 32901838

Similar Datasets

Project description:Previous studies have demonstrated that long non‑coding RNAs (lncRNAs) serve a key role in the development and progression of several types of cancer, including glioma. The lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) contributes to cancer growth through its effects on cell proliferation, migration, invasion and drug resistance. However, the exact regulatory mechanisms via which NEAT1 acts in glioma are unclear. In the present study, the expression levels and function of NEAT1 in glioma tissues and cell lines were examined in vitro and in vivo. By reverse transcription‑quantitative PCR and fluorescence in situ hybridization analysis, NEAT1 expression was upregulated in glioma tissues compared with in adjacent normal brain tissues, and elevated NEAT1 levels were associated with poor prognosis. Cell Counting Kit‑8, colony formation, ethynyldeoxyuridine, flow cytometry and western blotting assays were performed to detect the effects of NEAT1 on cell biological behavior. Knockdown of NEAT1 in glioma cell lines was associated with cell cycle arrest at the G0/G1 phase, decreased proliferation and elevated apoptosis in vitro, and resulted in reduced tumor growth and increased survival in a mouse xenograft model of glioma. Using bioinformatics analysis, RNA immunoprecipitation experiments and luciferase reporter assays, it was demonstrated that NEAT1 may competitively bind to microRNA (miR)‑324‑5p, thus blocking its interaction with target mRNAs. Potassium channel tetramerization protein domain containing 20 (KCTD20) was identified as a specific miR‑324‑5p target. Accordingly, the inhibition of NEAT1 resulted in the downregulation of KCTD20 through competitive binding with miR‑324‑5p, decreased cell proliferation and increased apoptosis. Concomitant NEAT1 knockdown and inhibition of miR‑324‑5p partially reversed the effects of NEAT1 knockdown on cell proliferation and apoptosis, and further regulated KCTD20 expression. Collectively, the present findings demonstrated that NEAT1 acted as a competing endogenous RNA for miR‑324‑5p, and identified the NEAT1/miR‑324‑5p/KCTD20 axis as a novel regulatory axis and a potential therapeutic target for human glioma.

Dataset Information

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.

Publications

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.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets