ArticleOncotarget2017
miR-338-3p inhibits epithelial-mesenchymal transition and metastasis in hepatocellular carcinoma cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Diagnostic significance and potential function of miR-338-5p in hepatocellular carcinoma: A bioinformatics study with microarray and RNA sequencing data.Molecular medicine reports · 2018Pooled it
- miRNA-338-3p influences the liver cancer stem cells and lenvatinib resistance properties by targeting SOX4.Scientific reports · 2025Article
- miR-383-3p and miR-6951-3p activate cell proliferation through the regulation of genes related to hypertelorism.Frontiers in cell and developmental biology · 2025Article
- hsa_circ_0000092 promotes hepatocellular carcinoma progression through up-regulating HN1 expression by binding to microRNA-338-3p.Journal of cellular and molecular medicine · 2024Article
- Circ_0124208 Promotes the Progression of Hepatocellular Carcinoma by Regulating the miR-338-3p/LAMC1 Axis.Molecular biotechnology · 2023Article
- Novel strategy of liver cancer treatment with modified antisense oligonucleotides targeting human vasohibin-2.Cancer science · 2023Article
- HIPK3 Circular RNA Promotes Metastases of HCC Through Sponging miR-338-3p to Induce ZEB2 Expression.Digestive diseases and sciences · 2021Article
- CircZNF609 promotes cell proliferation, migration, invasion, and glycolysis in nasopharyngeal carcinoma through regulating HRAS via miR-338-3p.Molecular and cellular biochemistry · 2021Article
- Modeling Liver Organogenesis by Recreating Three-Dimensional Collective Cell Migration: A Role for TGFβ Pathway.Frontiers in bioengineering and biotechnology · 2021Article
- SNHG16 promotes tumorigenesis and cisplatin resistance by regulating miR-338-3p/PLK4 pathway in neuroblastoma cells.Cancer cell international · 2020Article
- Article
- Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma.PeerJ · 2019Article
- Long non-coding RNA DSCAM-AS1 accelerates the progression of hepatocellular carcinoma via sponging miR-338-3p.American journal of translational research · 2019Article
- Cancer Associated Fibroblasts: Naughty Neighbors That Drive Ovarian Cancer Progression.Cancers · 2018Review
- MicroRNAs and clinical implications in hepatocellular carcinoma.World journal of hepatology · 2017Article
- Polymorphisms and expression pattern of circular RNA circ-ITCH contributes to the carcinogenesis of hepatocellular carcinoma.Oncotarget · 2017Article
- The EGFR/miR-338-3p/EYA2 axis controls breast tumor growth and lung metastasis.Cell death & disease · 2017Article
- Implication of the Hedgehog pathway in hepatocellular carcinoma.World journal of gastroenterology · 2017Review
- IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition.Oncology letters · 2017Article
- MicroRNA-338-3p inhibits thyroid cancer progression through targeting AKT3.American journal of cancer research · 2017Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down-regulation of the miRNA miR-338-3p correlates with the invasive ability of hepatocellular carcinoma (HCC) cells. However, it is currently unclear whether down-regulation of miR-338-3p induces epithelial-mesenchymal transition (EMT), which may be the underlying mechanism governing HCC invasion. Here, we demonstrate that restoration of miR-338-3p expression via transfection of a miR-338-3p mimic reversed EMT and inhibited the motility and invasiveness of HCC cells. Conversely, silencing of endogenous miR-338-3p expression with a miR-338-3p-specific inhibitor induced EMT and enhanced HCC cell motility. Additionally, Snail1 (an upstream regulatory protein of EMT) and Gli1 (a key transcription factor in the sonic hedgehog (SHH) signaling pathway) expression was up-regulated in cells treated with the miR-338-3p inhibitor and down-regulated by the miR-338-3p mimic. Further analyses demonstrated that miR-338-3p inhibitor-induced EMT in HCC cells was blocked by treatment with a small interfering RNA (siRNA) targeting Snail1, that the SHH signaling pathway was required for both miR-338-3p inhibitor-induced EMT and up-regulation of Snail1, and that miR-338-3p targeted a sequence within the 3'-untranslated region of N-cadherin mRNA. Notably, miR-338-3p expression was significantly down-regulated in HCC samples from patients with metastases and was associated with poor metastasis-free survival rates. Lastly, correlations between the expression levels of miR-338-3p and E-cadherin, Smoothened (SMO), Gli1, Snail1, N-cadherin, and vimentin were confirmed in HCC xenograft tumors and HCC patient specimens. Our findings suggest that miR-338-3p suppresses EMT and metastasis via both inhibition of the SHH/Gli1 pathway and direct binding of N-cadherin. miR-338-3p is a potential therapeutic target for metastatic HCC.
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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.