ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
miR-106a* inhibits the proliferation of renal carcinoma cells by targeting IRS-2.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Development and validation of a mitotic catastrophe-related genes prognostic model for breast cancer.PeerJ · 2024Article
- Overview of miR-106a Regulatory Roles: from Cancer to Aging.Bioengineering (Basel, Switzerland) · 2023Review
- Integrative analysis of miRNA and mRNA profiles reveals that gga-miR-106-5p inhibits adipogenesis by targeting the KLF15 gene in chickens.Journal of animal science and biotechnology · 2022Article
- Circulating Non-coding RNAs in Renal Cell Carcinoma-Pathogenesis and Potential Implications as Clinical Biomarkers.Frontiers in cell and developmental biology · 2020Review
- Article
- miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2).Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Epigenetics in renal cell cancer: mechanisms and clinical applications.Nature reviews. Urology · 2018Review
- MiR-106a* inhibits oral squamous cell carcinoma progression by directly targeting MeCP2 and suppressing the Wnt/β-Catenin signaling pathway.American journal of translational research · 2018Article
- MiR-106a-5p inhibits the cell migration and invasion of renal cell carcinoma through targeting PAK5.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs play critical roles in the development and progression of human cancers. Although it has been reported that miR-106a* is downregulated in follicular lymphoma, its role in renal cell carcinoma (RCC) remains unknown. This study investigated the expression and role of miR-106a* in human RCC. Our results showed that the miR-106a* expression decreased dramatically in clinical RCC tissues and cell lines. In vitro, overexpression of miR-106a* suppressed RCC cell proliferation and S/G2 transition, whereas inhibition of miR-106a* promoted cell proliferation and S/G2 transition. It was also found that miR-106a* expression was inversely correlated with the expression of insulin receptor substrate 2 (IRS-2). IRS-2 was determined to be a direct target of miR-106a* by a luciferase reporter assay. Importantly, silencing IRS-2 resulted in the same biologic effects as those of miR-106a* overexpression in RCC cells, including inhibition of RCC cell proliferation and triggering of S/G2 cell cycle arrest with inhibition of the PI3K/Akt signaling pathway. These results indicate that miR-106a* affects RCC progression by targeting IRS-2 with suppression of the PI3K/Akt signaling pathway in RCC cells. The findings suggest miR-106a* as a novel strategy for RCC treatment.
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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.