ArticleBioengineered2022
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.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- LncRNA EBLN3P Facilitates Osteosarcoma Metastasis by Enhancing Annexin A3 mRNA Stability and Recruiting HuR.Annals of surgical oncology · 2023Article
- Article
- MicroRNAs and Gene Regulatory Networks Related to Cleft Lip and Palate.International journal of molecular sciences · 2023Review
- Heavy Ion-Responsive lncRNA EBLN3P Functions in the Radiosensitization of Non-Small Cell Lung Cancer Cells Mediated by TNPO1.Cancers · 2023Article
- 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.Frontiers in genetics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.