ArticleMolecular medicine reports2022
MicroRNA‑671‑5p inhibits cell proliferation, migration and invasion in non‑small cell lung cancer by targeting MFAP3L.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
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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
11 citing papers in PubMed, 15 citations in OpenAlex.
- Caloric restriction modifies small RNA profiles and engages age-related molecular pathways in the CALERIE trial.iScience · 2026Article
- Article
- The PVT1-214/miR-671-5p/SLC45A4 signaling axis regulates cell proliferation in human gastric cancer.World journal of surgical oncology · 2025Article
- Neuroprotective effects of phytochemicals through autophagy modulation in ischemic stroke.Inflammopharmacology · 2025Review
- MicroRNA‑373‑3p inhibits the proliferation and invasion of non‑small‑cell lung cancer cells by targeting the GAB2/PI3K/AKT pathway.Oncology letters · 2024Article
- The pathogenic mechanism of syndactyly type V identified in a Hoxd13Q50R knock-in mice.Bone research · 2024Article
- Article
- MiRNAs in Lung Cancer: Diagnostic, Prognostic, and Therapeutic Potential.Diagnostics (Basel, Switzerland) · 2022Review
- Research progress on the role and mechanism of miR-671 in bone metabolism and bone-related diseases.Frontiers in oncology · 2022Review
- A review on the role of miR-671 in human disorders.Frontiers in molecular biosciences · 2022Review
- Association between microRNA 671 polymorphisms and the susceptibility to soft tissue sarcomas in a Chinese population.Frontiers in oncology · 2022Article
Corrections and comments
- Retraction · 2024-04-15Concerns/Issues about Data · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Manipulation of Data · Plagiarism of Data · · See also: https://pubpeer.com/publications/E86A6C16D80C7D257A98513A573D93
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miR)‑671‑5p serves as a tumor suppressor in several types of cancer, including gastric and breast cancer. However, the function of miR‑671‑5p in non‑small cell lung cancer (NSCLC) has not been described in detail. The present study aimed to investigate the role of miR‑671‑5p in NSCLC. The expression levels of miR‑671‑5p were determined in NSCLC tissue samples and cell lines using reverse transcription‑quantitative PCR. Prediction of miR‑671‑5p targets was performed using the TargetScan database and verified by luciferase reporter assay and western blot analysis. Functional experiments, including Cell Counting Kit‑8, wound healing and Transwell assays, were performed in NSCLC cells. The results of the present study demonstrated that lower expression levels of miR‑671‑5p were observed in NSCLC tissues and cell lines compared with those in the corresponding controls. Low miR‑671‑5p levels were significantly associated with an advanced Tumor‑Node‑Metastasis stage and lymph node metastasis in patients with NSCLC. Microfibril‑associated protein 3‑like (MFAP3L) was confirmed to be a direct target of miR‑671‑5p. The proliferative, migratory and invasive abilities of NSCLC cells were suppressed following transfection with miR‑671‑5p mimics and promoted by the miR‑671‑5p inhibitor compared with those in the respective control groups. In addition, the effects of miR‑671‑5p on cell proliferation, migration and invasion, as well as the expression levels of proliferating cell nuclear antigen, E‑cadherin, N‑cadherin and vimentin were reversed by MFAP3L overexpression. In conclusion, targeting the miR‑671‑5p/MFAP3L signaling pathway may be a promising therapeutic strategy for NSCLC treatment.
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