ArticleMolecular medicine reports2017
MicroRNA‑497 inhibits cellular proliferation, migration and invasion of papillary thyroid cancer by directly targeting AKT3.
Article in Molecular medicine reports, 2017. 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 It has been retracted, and should not be counted.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 12 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
12 citing papers in PubMed, 19 citations in OpenAlex.
- MicroRNAs as the critical regulators of cell migration and invasion in thyroid cancer.Biomarker research · 2022Review
- Article
- MicroRNAs in Papillary Thyroid Cancer: What Is New in Diagnosis and Treatment.Frontiers in oncology · 2021Review
- Regulation of microRNA-497 expression in human cancer.Oncology letters · 2021Review
- Article
- MicroRNA-203 restrains epithelial-mesenchymal transition, invasion and migration of papillary thyroid cancer by downregulating AKT3.Cell cycle (Georgetown, Tex.) · 2020Article
- Prognostic values and prospective pathway signaling of MicroRNA-182 in ovarian cancer: a study based on gene expression omnibus (GEO) and bioinformatics analysis.Journal of ovarian research · 2019Article
- MiR-16-5p inhibits breast cancer by reducing AKT3 to restrain NF-κB pathway.Bioscience reports · 2019Article
- Down-regulatedBioscience reports · 2019Article
- MicroRNA-16 functions as a tumor-suppressor gene in oral squamous cell carcinoma by targeting AKT3 and BCL2L2.Journal of cellular physiology · 2018Article
- Downregulation of miR‑486‑5p in papillary thyroid carcinoma tissue: A study based on microarray and miRNA sequencing.Molecular medicine reports · 2018Article
- Exosomal microRNA Therapy for Non-Small-Cell Lung Cancer.Technology in cancer research & treatmentReview
Corrections and comments
- Retraction · 2022-09-07Concerns/Issues about Data · Duplication of/in Image · Investigation by Third Party · Paper Mill · · see also: https://pubpeer.com/publications/943361CACB0C73D23B561359DD0730
- Retracted
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid cancer is the most common tumor of the endocrine organs. Emerging studies have indicated the critical roles of microRNAs (miRs) in papillary thyroid cancer (PTC) formation and progression through function as tumor suppressors or oncogenes. The present study investigated the expression level and biological roles of miR‑497 in PTC and its underlying mechanisms. It was demonstrated that the expression level of miR‑497 was reduced in both PTC tissues and cell lines. Enforced expression of miR‑497 suppressed PTC cell proliferation, migration and invasion. According to bioinformatics analysis, a luciferase reporter assay, reverse transcription‑quantitative polymerase chain reaction and western blotting, RAC‑γ serine/threonine‑protein kinase (AKT3) was demonstrated to be the direct target gene of miR‑497. In addition, AKT3 expression increased in PTC tissues and negatively correlated with miR‑497 expression. Furthermore, downregulation of AKT3 also suppressed cell proliferation, migration and invasion of PTC, which had similar roles to miR‑497 overexpression in PTC cells. Taken together, these results suggested that this newly identified miR‑497/AKT3 signaling pathway may contribute to PTC occurrence and progression. These findings provide novel potential therapeutic targets for the therapy of PTC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.