ArticleJournal of oncology2022
miR-3651 Participates in the Growth Cycle of Hepatocellular Carcinoma Cells and Promotes the Malignant Metastasis via the PI3K/AKT/mTOR Signalling Pathway.
Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Regulatory Effect of Non-Coding RNAs on Programmed Cell Death in Melanoma: Novel Therapeutic Crosstalk for Targeted Therapy.Current cancer drug targets · 2026Review
- The functional mechanism and clinical significance of miR-3651 in the healing process of Pilon fractures.Journal of orthopaedic surgery and research · 2025Article
- Relationship between specific microRNA expression and radioresistant conditions in HL60 acute myeloid leukemia cells.Molecular medicine reports · 2025Article
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Circulating miRNAs drive personalized medicine based on subgroup classification in myasthenia gravis patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Hepatocellular carcinoma (HCC) shows a growing incidence over the past few years, and clinical efforts are made to search for more effective novel diagnosis and therapy regimen for it to improve its outcome. This study probed into the association of miR-3651 with the PI3K/AKT/mTOR pathway to offer a more detailed reference to the follow-up exploration of novel diagnosis and therapy methods of HCC. Methods: Totally, 83 patients with HCC treated in our hospital between Apr. 2017 and Aug. 2018, 100 patients with simple liver cirrhosis (LC), and 94 normal persons over the same time span were enrolled, and serum miR-3651 in them was quantified to understand the predictive and prognostic significance of miR-3651 for HCC. In addition, with purchased human HCC cell strains (HepG2), the impacts of miR-3651 on the invasion as well as proliferation of HepG2 were determined using the MTT and Transwell assays, and the PI3K/AKT/mTOR pathway and autophagy-associated proteins in HepG2 were quantified via WT. Results: Serum miR-3651 was found to be higher in HCC patients than in LC patients and normal persons, and it presented a sensitivity and specificity of 57.14% and 94.00%, respectively, in forecasting the occurrence of HCC in LC patients. The decrease of miR-3651 in HCC patients after therapy was strongly bound up with patients' prognosis, and its increase implied an increased risk of death. In Conclusion: miR-3651 intensifies the growth and invasion of HCC cells through activating the PI3K/AKT/mTOR signalling pathway, which is probably a breakthrough in the future diagnosis and therapy of HCC.
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.