The biological function of the long non-coding RNA endogenous born avirus-like nucleoprotein in lung adenocarcinoma is mediated through the microRNA-655-3p/B-cell lymphoma-2 axis

Abstract

Lung adenocarcinoma (LUAD) is a subtype of lung cancer, and therapy remains a great challenge. A growing body of evidence shows that long-chain non-coding RNAs (lncRNAs) play an important role in the occurrence and development of LUAD. This study investigated the roles and mechanisms of action of EBLN3P in LUAD. The bioinformatics software starBase and TargetScan were used to predict the binding sites of the lncRNA endogenous born avirus-like nucleoprotein (EBLN3P) and microRNA (miR)-655-3p in LUAD. The regulatory role of EBLN3P and miR-655-3p in cell proliferation was verified through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H-tetrazolium bromide (MTT) assay. The binding sites between EBLN3P, miR-655-3p, and B-cell lymphoma-2 (Bcl-2) were assessed using dual-luciferase reporter assay, western blotting, and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Flow cytometry (FCM) was performed to analyze the apoptotic rates of A549 cells after transfection. The results revealed that EBLN3P was upregulated, whereas miR-655-3p was downregulated in LUAD cell lines (A549 and NCI-H23). Bioinformatics analysis and dual-luciferase reporter assays indicated that EBLN3P interacted with miR-655-3p. Knockdown of EBLN3P notably inhibited the bioactivity and induced apoptosis in A549 cells by upregulating miR-655-3p. Mechanistically, miR-655-3p inhibits cell viability and induces apoptosis by inhibiting Bcl-2 expression. The high expression of Bcl-2 reversed the impact of miR-655-3p on the inhibition of cell bioactivity and induction of apoptosis in A549 cells. In conclusion, this study demonstrated that EBLN3P silencing inhibits bioactivity and induces apoptosis via the miR-655-3p/Bcl-2 axis, providing a potential therapeutic target for lung adenocarcinoma.

Heavy Ion-Responsive lncRNA EBLN3P Functions in the Radiosensitization of Non-Small Cell Lung Cancer Cells Mediated by TNPO1

“…Recent studies have demonstrated that lncRNAs are crucial regulators of tumor growth and invasion; they have reported that LNC EBLN3P can function as an oncogene in osteosarcoma and lung adenocarcinoma, and the inhibition of EBLN3P can be used in the treatment of cancer [14,15]. LNC EBLN3P can also promote the recovery of impaired spiral ganglion neurons by regulating the miR-204-5p/TMPRSS3 axis [16].…”

Integrative analysis of the expression profiles of whole coding and non-coding RNA transcriptomes and construction of the competing endogenous RNA networks for chronic obstructive pulmonary disease

“…Similarly, the expression of the NORAD was notably increased in cancer tissues and cells compared with that in normal tissues and cells in NSCLC, which regulates the proliferation, migration, and invasion capabilities of NSCLC cells by targeting the miR-520a-3p/PI3k/Akt/mTOR signaling pathways ( Wan et al, 2020 ). Wang et al revealed that the lncRNA, EBLN3P, was upregulated in lung adenocarcinoma cell lines (A549 and NCI-H23), inhibiting A549 cell viability and promoting apoptosis via the miR-655-3p/Bcl-2 axis ( Wang and Yin, 2022 ). CircRNA is a covalently closed loop-like structure that is highly specific to the eukaryotic transcriptome and can be used as a microRNA sponge, a splicer, and for transcribed gene expression ( Qu et al, 2015 ).…”

LncRNA EBLN3P Facilitates Osteosarcoma Metastasis by Enhancing Annexin A3 mRNA Stability and Recruiting HuR

“…Furthermore, EBLN3P can modulate the proliferation of lung adenocarcinoma cells through the miR-655-3p/Bcl2 axis. 36 Knockdown of EBLN3P hinders the proliferation, invasion, and migration of Jurkat cells by increasing miR-655-3p expression. 37 As for HuR, there is evidence that HuR-RNA interactions play essential roles in cancer treatment.…”