ArticleJournal of Cancer2020
High-matrix-stiffness induces promotion of hepatocellular carcinoma proliferation and suppression of apoptosis via miR-3682-3p-PHLDA1-FAS pathway.
Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- The Stiff Side of Cancer: How Matrix Mechanics Rewrites Non-Coding RNA Expression Programs.Non-coding RNA · 2026Review
- Forcing the code: tension modulates signaling to drive morphogenesis and malignancy.Genes & development · 2025Review
- Expanding on roles of pleckstrin homology-like domain family A member 1 protein.Cell and tissue research · 2025Review
- NRF1-Induced lncRNA DDX11-AS1 Contributes to the Progression of Hepatocellular Carcinoma via Activating CA9 Expression and the MEK/ERK Pathway.Journal of hepatocellular carcinoma · 2025Article
- MicroRNAs in Hepatocellular Carcinoma Pathogenesis: Insights into Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- The impact of matrix stiffness on hepatic cell function, liver fibrosis, and hepatocellular carcinoma-Based on quantitative data.Biophysics reviews · 2024Review
- Matrix Stiffness Regulated Endoplasmic Reticulum Stress-mediated Apoptosis of Osteosarcoma Cell through Ras Signal Cascades.Cell biochemistry and biophysics · 2023Article
- A biomechanical view of epigenetic tumor regulation.Journal of biological physics · 2023Review
- Tumor matrix stiffness provides fertile soil for cancer stem cells.Cancer cell international · 2023Review
- Mechanical Regulation of Mitochondrial Dynamics and Function in a 3D-Engineered Liver Tumor Microenvironment.ACS biomaterials science & engineering · 2023Article
- Contribution of mechanical homeostasis to epithelial-mesenchymal transition.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- miR-3682-3p directly targets FOXO3 and stimulates tumor stemness in hepatocellular carcinomaWorld journal of stem cells · 2022Article
- Dysregulation of miR-577, miR-505-3p, miR-3682-3p, and miR-4661 in Breast Cancer Patients Based on Estrogen Receptor Status : Dysregulation of miRNAs in Breast Cancer Patients Based on ER Status.Galen medical journal · 2022Article
- [High expression of miR-3682-3p is an unfavorable prognostic factor of hepatocellular carcinoma].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Hypoxia-induced cofilin 1 promotes hepatocellular carcinoma progression by regulating the PLD1/AKT pathway.Clinical and translational medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) with malignant behaviors related to death causes distant metastasis and is the fourth primary cancer in the whole world, which has taken millions lives in Asian countries such as China. The novel miR-3682-3p involving high-expression-related poor prognosis in HCC tissues and cell lines indicate oncogenesis functions in vitro and in vivo. According to TCGA database, our group find several none-coding RNAs showing abnormal expression including miR-3682-3p, thus we originally confirmed the inhibition of proliferation and acceleration of apoptosis are enhanced in miR-3682-3p knock-down cell lines. Then, in nude mice transplantation assays, we found the suppressor behaviors, smaller nodules and lower speed of tumor expansion in model of injection of cell cultured and transfected shRNA-miR-3682-3p. A combination of databases (Starbase, Targetscan and MiRgator) illustrates miR-3682-3p targets PHLDA1, which shows negative correlation demonstrated by dual-luciferase reporter system. To make functional verification of PHLDA1, we upregulate the gene and rescue tests are established to confirm that miR-3682-3p suppresses PHLDA1 to promotion of cell growth. Rescue experiments finish making confirmation of relation of miR-3682-3p and PHLDA1 subsequently. Cirrhotic tissues illustrate strong correlation to higher miR-3682-3p and clinical features make the hint that high-extracellular-matrix-stiffness environment promotes such miRNA. Functional tests on different stiffness provide the proof of underlying mechanism. In conclusion, the overexpression of miR-3682-3p mediates PHLDA1 inhibition could impede apoptosis and elevate proliferation of HCC through high-extracellular-matrix-stiffness environment potentially.
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Registered trials
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