ArticlePloS one2023
Hsa-miR-22-3p inhibits liver cancer cell EMT and cell migration/ invasion by indirectly regulating SPRY2.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Downregulation of circulating miR-22 and elevation of serum ATP-citrate lyase in colorectal cancer: a proof-of-concept study.Molecular biology reports · 2026Article
- Extracellular Vesicle and Plasma miRNAs as Candidate Biomarkers of Traumatic Brain Injury in the Context of Polytrauma.International journal of molecular sciences · 2026Article
- Rewiring miR-22/SNAI1 via CRISPR-based edge editing destabilizes the epithelial phenotype.NPJ systems biology and applications · 2026Article
- Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Per- and polyfluoroalkyl substances (PFAS) and microRNA: An epigenome-wide association study in firefighters.Environmental research · 2025Article
- MicroRNA Signatures in Dental Pulp Stem Cells Following Nicotine Exposure.Dentistry journal · 2025Article
- MiR-22/GLUT1 Axis Induces Metabolic Reprogramming and Sorafenib Resistance in Hepatocellular Carcinoma.International journal of molecular sciences · 2025Article
- Fecal miRNA Profiling of Yorkshire Terrier Enteropathy.International journal of molecular sciences · 2025Article
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- The Role of microRNA-22 in Metabolism.International journal of molecular sciences · 2025Review
- Comprehensive investigation of matrix metalloproteinases in skin cutaneous melanoma: diagnostic, prognostic, and therapeutic insights.Scientific reports · 2025Article
- A migrasome-related lncRNA signature predicts prognosis and immune response in hepatocellular carcinoma: Implications for biomarker discovery and therapeutic targeting.Frontiers in pharmacology · 2025Article
- Epigenetic crosstalk between stem cells and tumors: mechanisms and emerging perspectives.American journal of stem cells · 2025Review
- Review of the Different Outcomes Produced by Genetic Knock Out of the Long Non-coding microRNA-host-gene MIR22HGMicroRNA (Shariqah, United Arab Emirates) · 2025Review
- Advances in the study of the mechanism of action of miR‑22 in liver lesions (Review).Oncology letters · 2024Review
- The role of CBL family ubiquitin ligases in cancer progression and therapeutic strategies.Frontiers in pharmacology · 2024Review
- Article
- The pivotal role of EMT-related noncoding RNAs regulatory axes in hepatocellular carcinoma.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The general mechanism for microRNAs to play biological function is through their inhibition on the expression of their target genes. In cancer, microRNAs may accelerate cell senescence, block angiogenesis, decrease energy supplies, repress tumor cell cycle and promote apoptosis to function as the tumor repressors. On the other hand, microRNAs can modulate tumor suppressor molecules to activate oncogene relevant signaling pathway to initiate tumorigenesis and promote tumor progression. By targeting different genes, miR-22 can function as either a tumor suppressor or a tumor promoter in different types of cancer. In liver cancer, miR-22 mainly functions as a tumor suppressor via its regulation on different genes. In this study, we demonstrated that miR-22 indirectly regulates SPRY2 by inhibiting CBL, an E3 ligase for SPRY2 that has been confirmed. As one of the modulators of the MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) signaling pathway, SPRY2 plays important roles in many developmental and physiological processes, and its deregulation has been reported in different types of cancer and shown to affect cancer development, progression, and metastasis. By inhibiting the expression of CBL, which stabilizes SPRY2, miR-22 indirectly upregulates SPRY2, thereby suppressing the epithelial-mesenchymal transition (EMT), cell migration, and invasion and decreasing the expression of liver cancer stem cell (CSC) marker genes. The inhibitory effects of miR-22 on EMT, cell migration, and invasion can be blocked by the knockdown of SPRY2 expression in miR-22 overexpressing cells. Additionally, we demonstrated that miR-22 expression inhibits the ERK signaling pathway and that this effect is due to its upregulation of SPRY2. Overall, our study revealed a novel miR-22-3p/CBL/SPRY2/ERK axis that plays an important role in EMT, cell migration, and invasion of liver cancer cells.
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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 Socratic graph.