Aim Recent reports of potential harmful effects of nonsteroidal anti‐inflammatory drugs (NSAIDs) in treating patients with coronavirus disease 2019 (COVID‐19) have raised great concern. Methods We searched the PubMed, EMBASE, Cochrane Library and MedRxiv databases to examine the prevalence of NSAID use and associated COVID‐19 risk, outcomes and safety. Results Twenty‐five studies with a total of 101 215 COVID‐19 patients were included. Prevalence of NSAID use among COVID‐19 patients was 19% (95% confidence interval [CI] 14‐23%, no. of studies [n] = 22) and NSAID use prior to admission or diagnosis of COVID‐19 was not associated with an increased risk of COVID‐19 (adjusted odds ratio [aOR] = 0.93, 95% CI 0.82‐1.06, I 2 = 34%, n = 3), hospitalization (aOR = 1.06, 95% CI 0.76‐1.48, I 2 = 81%, n = 5), mechanical ventilation (aOR = 0.71, 95% CI 0.47‐1.06, I 2 = 38%, n = 4) or length of hospital stay. Moreover, prior use of NSAIDs was associated with a decreased risk of severe COVID‐19 (aOR = 0.79, 95% CI 0.71‐0.89, I 2 = 0%, n = 7) and death (aOR = 0.68, 95% CI 0.52‐0.89, I 2 = 85%, n = 10). Prior NSAID administration might also be associated with an increased risk of stroke (aOR = 2.32, 95% CI 1.04‐5.2, I 2 = 0%, n = 2), but not myocardial infarction (aOR = 1.49, 95% CI 0.25‐8.92, I 2 = 0, n = 2) and composite thrombotic events (aOR = 1.56, 95% CI 0.66‐3.69, I 2 = 52%, n = 2). Conclusion Based on current evidence, NSAID use prior to admission or diagnosis of COVID‐19 was not linked with increased odds or exacerbation of COVID‐19. NSAIDs might provide a survival benefit, although they might potentially increase the risk of stroke. Controlled trials are still required to further assess the clinical benefit and safety (e.g., stroke and acute renal failure) of NSAIDs in treating patients with COVID‐19.

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As a component of the spliceosome, U1 small nuclear ribonucleoproteins (U1RNPs) play critical roles in RNA splicing, and recent studies have shown that U1RNPs could recruit long non-coding RNAs (lncRNAs) to chromatin which are involved in cancer development. However, the interplay of U1 snRNP, lncRNAs and downstream genes and signaling pathways are insufficiently understood in hepatocellular carcinoma (HCC). The expression of U1RNPs was found to be significantly higher in tumors than normal tissues in liver hepatocellular carcinomas of The Cancer Genome Atlas (TCGA-LIHC) dataset. LncRNAs with potential U1-binding sites (termed U1-lncRNAs) were found to be mostly located in the nucleus and their expression was higher in tumor than in normal tissues Bioinformatic analysis indicated that U1-lncRNAs worked with RNA-binding proteins and regulated the transcription cycle in HCC. A U1-lncRNA risk model was constructed using a TCGA dataset, and the AUCs of this risk model to predict 1-, 3- and 5-year overall survival were 0.82, 0.84 and 0.8, respectively. Furthermore, silencing of the small nuclear ribonucleoprotein D2 polypeptide (SNRPD2) resulted in impaired proliferation, G1/M cell cycle arrest and downregulation of transcription-cycle-related genes in HCC cell lines. Taken together, these results indicate that U1RNPs interact with lncRNAs and promote the transcription cycle process in HCC, which suggests that these could be novel biomarkers in the clinical management of HCC.

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