ArticleHeliyon2024
Long noncoding RNA LINC00858 aggravates the progression of esophageal squamous cell carcinoma via regulating the miR-425-5p/ABL2 axis.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Functions and mechanisms of long non-coding RNA in esophageal squamous cell carcinoma (Review).Oncology letters · 2025Review
- A novel necroptosis-related miRNA signature for predicting the prognosis of esophageal cancer and immune infiltration analysis.Translational cancer research · 2025Article
- A Comprehensive Review of Protein Biomarkers for Invasive Lung Cancer.Current oncology (Toronto, Ont.) · 2024Review
- Roles of long non‑coding RNAs in esophageal cell squamous carcinoma (Review).International journal of molecular medicine · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most fatal cancers with high morbidity and mortality, which severely affects people's lives. Long intergenic non-protein coding RNA 858 (LINC00858) was confirmed to promote the progression of colorectal cancer and lung cancer. However, the role of lncRNA LINC00858 is still unknown in ESCC. Herein, the main purpose of research was to explore LINC00858 function and its impact on ESCC cell biological behaviors. RT-qPCR was used to test the expression of LINC00858, miR-425-5p and ABL proto-oncogene 2 (ABL2) in ESCC cells. Functional experiments such as EdU assay, CCK-8 assay, transwell assay and Western blot assay were conducted to investigate the biological behaviors of ESCC cells. Luciferase reporter assay and RIP assay were implemented to determine the binding situation among RNAs. LINC00858 expression was abnormally high in ESCC cells and down-regulation of LINC00858 could restrain the proliferation, invasion, migration and EMT process of ESCC cells. Furthermore, miR-425-5p was proved to be sponged by LINC00858 and was down-regulated in ESCC cells. Besides, we discovered that miR-425-5p could target ABL2. Moreover, knockdown of ABL2 reversed the promoting function of miR-425-5p inhibitor on ESCC progression. LINC00858 aggravated ESCC progression via regulating the miR-425-5p/ABL2 axis.
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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.