ArticleMolecular biotechnology2022
Let-7c-5p Restrains Cell Growth and Induces Apoptosis of Lung Adenocarcinoma Cells via Targeting ESPL1.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of subgroups and development of prognostic risk models along the glycolysis-cholesterol synthesis axis in lung adenocarcinoma.Scientific reports · 2024Article
- Article
- Sex differences in the tumor promoting effects of tobacco smoke in a cRaf transgenic lung cancer disease model.Archives of toxicology · 2024Article
- Exosomal microRNA let-7c-5p enhances cell malignant characteristics by inhibiting TAGLN in oral cancer.Oncology research · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is a predominant malignancy, and its high mortality prompts us to incessantly probe the relevant targeted treatment. This work intended to study the molecular mechanism of ESPL1 in LUAD. Bioinformatics analysis was performed for pan-cancer and prognosis analysis as well as target gene prediction. Expression of ESPL1 mRNA and let-7c-5p was determined via qRT-PCR, and western blot was employed to detect protein level of ESPL1. Dual-luciferase reporter gene method verified the interaction between ESPL1 and let-7c-5p. Thereafter, CCK-8, wound healing, Transwell, and flow cytometry assays were utilized to investigate proliferation, migration, and apoptosis of LUAD cells. The results revealed that ESPL1 was upregulated in LUAD, which was associated with poor prognosis. Overexpressed ESPL1 promoted LUAD cells to invade, proliferate, and migrate. Furthermore, ESPL1 was a target gene of let-7c-5p. Let-7c-5p was downregulated in LUAD cells, and played a suppressive role in LUAD malignant development, while reversed by ESPL1. Taken together, it was posited that let-7c-5p/ESPL1 may be underlying therapeutic targets of LUAD.
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