ArticleCell cycle (Georgetown, Tex.)2022
miR-29a-3p mitigates the development of osteosarcoma through modulating IGF1 mediated PI3k/Akt/FOXO3 pathway by activating autophagy.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- miRNA‑29a inhibits the proliferation of HUVECs by regulating the ITGB1/β‑catenin/c‑Myc pathway.Molecular medicine reports · 2026Article
- Natural products reshape osteosarcoma cell fate: promoting cell death.Frontiers in pharmacology · 2026Review
- LncRNA CRNDE ameliorates bone fracture by regulating cell viability and apoptosis of osteoblasts.Journal of orthopaedic surgery and research · 2025Article
- miR-29a-3p compositely regulates the COL6A6/PTEN-PI3K/Akt/CUX1 feedback loop to participate in the proliferation and invasion of pituitary adenomas.Journal of molecular histology · 2025Article
- Long non-coding RNA NEAT1 promotes ovarian granulosa cell proliferation and cell cycle progression via the miR-29a-3p/IGF1 axis.Journal of ovarian research · 2025Article
- Research Progress on Natural Products That Regulate miRNAs in the Treatment of Osteosarcoma.Biology · 2025Review
- Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024Article
- Interaction of ncRNAs and the PI3K/AKT/mTOR pathway: Implications for osteosarcoma.Open life sciences · 2024Review
- Autophagy Modulation as a Potential Therapeutic Strategy in Osteosarcoma: Current Insights and Future Perspectives.International journal of molecular sciences · 2023Review
- MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- PINK1 regulates apoptosis of osteosarcoma as the target gene of cisplatin.Journal of orthopaedic surgery and research · 2023Article
- Modulation of AKT Pathway-Targeting miRNAs for Cancer Cell Treatment with Natural Products.International journal of molecular sciences · 2023Review
- Functional role of MicroRNA/PI3K/AKT axis in osteosarcoma.Frontiers in oncology · 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
Osteosarcoma (OS), occurring in mesenchymal tissues and with a high degree of malignancy, is most common in children and adolescents. At present, we intend to figure out the expression and functions of miR-29a-3p in OS development. Reverse transcription-polymerase chain reaction (RT-PCR) was adopted to monitor the expression of miR-29a-3p and IGF1 in OS tissues and adjacent non-tumor tissues. Then, the 3- (4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, colony formation experiment, western blot and Transwell assay were conducted to validate OS cell proliferation, colony formation ability, apoptosis, migration and invasion. Next, the association between miR-29a-3p and IGF1 was corroborated by the dual-luciferase reporter assay and the Pearson correlation analysis. Finally, WB was implemented to test the levels of autophagy-related proteins LC3-I/LC3-II, Beclin-1, p62, and the IGF-1 R/PI3k/Akt/FOXO3 axis in OS cells. As a result, miR-29a-3p was down-regulated in OS tissues (versus adjacent non-tumor tissues) and OS cell lines. Overexpressing miR-29a-3p aggravated apoptosis, dampened cell proliferation, colony formation, migration and invasion, and promoted autophagy of OS cells. IGF1 was identified as a target of miR-29a-3p. IGF1 induced oncogenic effects in OS by activating IGF-1 R/ PI3k/Akt pathway, and it dampened the tumor-suppressive effect of miR-29a-3p on OS. Taken together, miR-29a-3p repressed the OS evolvement through inducing autophagy and inhibiting IGF1 mediated PI3k/Akt/FOXO3 pathway.
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.