Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma

Abstract

Long noncoding RNA SLC9A3 antisense RNA 1 (SLC9A3-AS1) plays a central role in lung cancer; yet, its functions in nasopharyngeal carcinoma (NPC) have not been elucidated. The present study revealed the roles of SLC9A3-AS1 in NPC and dissected the mechanisms downstream of SLC9A3-AS1. SLC9A3-AS1 levels in NPC were assessed by applying RT-qPCR. The modulatory role of SLC9A3-AS1 interference on NPC cells was examined using numerous functional experiments. High expression of SLC9A3-AS1 was observed in NPC samples. Patients with NPC with a high level of SLC9A3-AS1 experienced a shorter overall survival than those with a low SLC9A3-AS1 level. Loss of SLC9A3-AS1 reduced NPC cell proliferation, colony formation, migration, and invasion but induced cell apoptosis in vitro . Animal experiments further revealed that the depletion of SLC9A3-AS1 hindered NPC tumour growth in vivo . As a competitive endogenous RNA, SLC9A3-AS1 sponged microRNA-486-5p (miR-486-5p), consequently upregulating E2F transcription factor 6 (E2F6). Finally, the effects of SLC9A3-AS1 silencing on NPC cells were reversed by inhibiting miR-486-5p or overexpressing E2F6. In summary, SLC9A3-AS1 exerted carcinogenic effects on NPC cells by adjusting the miR-486-5p/E2F6 axis. Accordingly, the newly identified SLC9A3-AS1/miR-486-5p/E2F6 pathway may offer attractive therapeutic targets for future development.

An Integrated Analysis of mRNAs and miRNAs Microarray Profiles to Screen miRNA Signatures Involved in Nasopharyngeal Carcinoma

“…Overwhelming evidence has demonstrated that miRNA let-7 family (-a, -b, -c, -d, -e, -f, -g and -i) exerted regulatory roles at the transcriptional and post-transcriptional levels among species and their aberrant expression might be closely linked with the pathogenesis of cancers such as NPC. 29,30 Luan et al conducted a metaanalysis of 8 miRNA studies for NPC and pointed out that let-7d was remarkably decreased in NPC tumor tissues, which was consistent with our results from bioinformatics analysis. 31 Similarly, Wong et al previously also found that there were lower levels of let-7d and let-7f in NPC cells than normal epithelial cells according to the real-time quantitative PCR, More interestingly, they suggested that increased let-7 levels could down-regulate the MYC protein expression in NPC cell lines.…”

Identification of important modules and biomarkers in tuberculosis based on WGCNA

“…In addition, KEGG analysis showed that the blue module was significantly enriched in infection and immunity-related processes, including autophagy and apoptosis. Some lncRNAs in the blue module in our study, have been previously confirmed to participate in apoptosis by experiments, including the promotion of apoptosis by lncRNA PAXIP1 (Ma and Zheng, 2021) and lncRNA SLC9A3 (Li et al, 2021), while the inhibition of apoptosis by lncRNA EZR-AS1 (Yu et al, 2023). Meanwhile, recent studies have also shown that lncRNA EGOT (Liu et al, 2020) can inhibit autophagy, either by ceRNA interactive patterns or by posttranscriptional regulation of the ATG7/16 L1 (Wang I. K. et al, 2020).…”

lncRNA SLC9A3-AS1 Promotes Oncogenesis of NSCLC via Sponging microRNA-760 and May Serve as a Prognosis Predictor of NSCLC Patients

“…Recently, SLC9A3-AS1 has been identified as an oncogene in nasopharyngeal carcinoma. 15 Bai et al also preliminarily uncovered the biomarker role of SLC9A3-AS1 in LC. 14 However, the full-scale role of SLC9A3-AS1 in the oncogenesis and progression of NSCLC remains undefined.…”

“… 14 Recently, Li et al reported that lncRNA SLC9A3-AS1 promoted the oncogenesis of nasopharyngeal carcinoma by modulating the miR-486-5p/E2F transcription factor 6 axis. 15 Given the upregulation and discrimination power of SLC9A3-AS1 in LC patients, we further speculated that SLC9A3-AS1 might play a central role during the oncogenesis of NSCLC.…”