ArticleHeliyon2023
MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 6 citations in OpenAlex.
- LncRNA MCF2L-AS1 inhibits neuronal damage induced by 1-methyl-4-phenylpyridinium (MPP+) via regulating miR-28-5p.Journal of neurovirology · 2025Article
- Unraveling epigenomic signatures and effectiveness of electroconvulsive therapy in treatment-resistant depression patients: a prospective longitudinal study.Clinical epigenetics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Long noncoding RNA (lncRNA) is widely acknowledged for its crucial role in the biological processes of various human cancers. MCF2L antisense RNA 1 (MCF2L-AS1) is a newly identified lncRNA, which remains unexplored in the context of cancer. Methods: MCF2L-AS1 expression was examined using qRT-PCR analysis. The impact of MCF2L-AS1 on LUAD cell growth was assessed through CCK-8, colony formation, EdU, caspase-3 activity, TUNEL, Western blot, and transwell assays. The interaction between miR-874-3p and MCF2L-AS1 or STAT3 was confirmed by RIP, luciferase reporter, and RNA pull-down assays. Results: Our study demonstrated the overexpression of MCF2L-AS1 in LUAD cells. Functionally, the silencing of MCF2L-AS1 hindered cell proliferation, migration, and invasion, while promoting cell apoptosis. Notably, the depletion of MCF2L-AS1 was associated with decreased cisplatin resistance. Mechanistically, MCF2L-AS1 was identified as an upstream gene of miR-874-3p, negatively regulating its expression. Following this, STAT3, the downstream target of miR-874-3p, was identified. Additionally, the expression of STAT3 was inversely related to miR-874-3p and positively regulated by MCF2L-AS1. A restoration assay suggested that MCF2L-AS1 promoted LUAD cell growth by sponging miR-874-3p and modulating STAT3 expression. Intriguingly, STAT3 was subsequently confirmed as a transcription factor that binds to the MCF2L-AS1 promoter, thereby enhancing its transcription. Conclusions: The MCF2L-AS1/miR-874-3p/STAT3 feedback loop plays a significant role in LUAD cell growth and cisplatin resistance.
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.