ArticleAnnals of translational medicine2021
miR-126-3p contributes to sorafenib resistance in hepatocellular carcinoma via downregulating SPRED1.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis.iScience · 2026Article
- Translational insights into miR-126 and miR-423: biomarkers and therapeutic targets in cancer, cardiovascular, metabolic and kidney diseases.Frontiers in molecular biosciences · 2026Review
- Targeting Kinase Suppressor of Ras 1 (KSR1) for Cancer Therapy.Pharmaceutics · 2025Review
- The role of SPRED1 mutation in melanoma.European journal of medical research · 2025Review
- Dysregulation of MicroRNAs in Hepatocellular Carcinoma: Targeting Oncogenic Signaling Pathways for Innovative Therapies.International journal of molecular sciences · 2025Review
- MicroRNAs in Hepatocellular Carcinoma Pathogenesis: Insights into Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Prediction of CAF-related genes in immunotherapy and drug sensitivity in hepatocellular carcinoma: a multi-database analysis.Genes and immunity · 2024Article
- The interplay between noncoding RNAs and drug resistance in hepatocellular carcinoma: the big impact of little things.Journal of translational medicine · 2023Review
- Role of Some microRNA/ADAM Proteins Axes in Gastrointestinal Cancers as a Novel Biomarkers and Potential Therapeutic Targets-A Review.Current issues in molecular biology · 2023Review
- Extracellular vesicle‑mediated miR‑126‑3p transfer contributes to inter‑cellular communication in the liver tumor microenvironment.International journal of oncology · 2023Article
- circSMARCA5 Is an Upstream Regulator of the Expression of miR-126-3p, miR-515-5p, and Their mRNA Targets,International journal of molecular sciences · 2022Article
- Erratum to miR-126-3p contributes to sorafenib resistance in hepatocellular carcinoma via downregulating SPRED1.Annals of translational medicine · 2022Article
- miR-126-3p-loaded small extracellular vesicles secreted by urine-derived stem cells released from a phototriggered imine crosslink hydrogel could enhance vaginal epithelization after vaginoplasty.Stem cell research & therapy · 2022Article
- Low miR-10b-3p associated with sorafenib resistance in hepatocellular carcinoma.British journal of cancer · 2022Article
- CircLIFR suppresses hepatocellular carcinoma progression by sponging miR-624-5p and inactivating the GSK-3β/β-catenin signaling pathway.Cell death & disease · 2022Article
- Targeting non-coding RNAs to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2022Review
- Non-coding RNA in cancer drug resistance: Underlying mechanisms and clinical applications.Frontiers in oncology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSorafenib can prolong the survival of patients with advanced hepatocellular carcinoma (HCC). However, drug resistance remains the main obstacle to improving its efficiency. This study aimed to explore the likely molecular mechanism of sorafenib resistance.
methodsDifferentially expressed microRNAs (miRNAs) related to sorafenib response were analyzed with the Limma package in R software. The expression levels of miR-126-3p and sprouty-related EVH1 domain-containing protein 1 (SPRED1) in HCC cells were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cell viability and proliferation were detected with Cell Counting Kit-8 (CCK-8), EdU proliferation, and clone formation assays. Transwell assays were performed to measure cell migration and invasion. TargetScan, MicroRNA Target Prediction Database (miRDB), and StarBase v2.0 were used to predict the targets of miR-126-3p. SPRED1 was confirmed as a target gene of miR-126-3p by dual-luciferase reporter assay and Western blotting. Finally, the
resultsHCC cells with high expression of miR-126-3p exhibited increased resistance to sorafenib. The results of bioinformatics analysis and the dual-luciferase reporter assay showed that miR-126-3p directly targeted SPRED1. The sensitivity of HCC cells to sorafenib was markedly enhanced by SPRED1 upregulation. Gain- and loss-of function experiments verified that miR-126-3p induced sorafenib resistance in HCC through downregulating SPRED1. Furthermore, the inhibition of miR-126-3p markedly increased the effectiveness of sorafenib against HCC
conclusionsOur study demonstrates that regulating the miR-126-3p/SPRED1 axis might be a promising strategy for enhancing the antitumor effect of sorafenib in the treatment of HCC.
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