ArticleInternational journal of molecular sciences2012
miR-338-3p is down-regulated by hepatitis B virus X and inhibits cell proliferation by targeting the 3'-UTR region of CyclinD1.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Long non-coding RNA FOXD2-AS1 promotes inflammation but suppresses osteogenesis in pulpitis via miR-338-3p/THBS1 axis.Odontology · 2026Article
- miR-338-3p targets WAPL to suppress proliferation and invasion in cervical cancer cells: experimental insights.World journal of surgical oncology · 2025Article
- miRNA-338-3p influences the liver cancer stem cells and lenvatinib resistance properties by targeting SOX4.Scientific reports · 2025Article
- Reduced miR-338-3p contributes to polycystic ovarian syndrome by inhibiting proliferation and enhancing apoptosis.Hereditas · 2025Article
- miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Investigating Core Signaling Pathways of Hepatitis B Virus Pathogenesis for Biomarkers Identification and Drug Discovery via Systems Biology and Deep Learning Method.Biomedicines · 2020Article
- Review
- Review
- Long non-coding RNA NR2F1-AS1 promoted proliferation and migration yet suppressed apoptosis of thyroid cancer cells through regulating miRNA-338-3p/CCND1 axis.Journal of cellular and molecular medicine · 2019Article
- Molecular Mechanisms Driving Progression of Liver Cirrhosis towards Hepatocellular Carcinoma in Chronic Hepatitis B and C Infections: A Review.International journal of molecular sciences · 2019Review
- 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
- LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p.Journal of gynecologic oncology · 2018Article
- LncRNA ABHD11-AS1 promotes the development of endometrial carcinoma by targeting cyclin D1.Journal of cellular and molecular medicine · 2018Article
- MiR-494-3p promotes PI3K/AKT pathway hyperactivation and human hepatocellular carcinoma progression by targeting PTEN.Scientific reports · 2018Article
- HBeAg-induced miR-106b promotes cell growth by targeting the retinoblastoma gene.Scientific reports · 2017Article
- Hepatitis B virus X protein-mediated non-coding RNA aberrations in the development of human hepatocellular carcinoma.Experimental & molecular medicine · 2017Review
- Article
- Role of microRNAs in inflammation-associated liver cancer.Cancer biology & medicine · 2016Article
- miR-217 and CAGE form feedback loop and regulates the response to anti-cancer drugs through EGFR and HER2.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus X protein (HBx) is recognized as an oncogene in hepatocellular carcinoma (HCC). HBx regulates microRNA expression, including down-regulating miR-338-3p in LO2 cells. Here, we investigated miR-338-3p function in HBx-mediated hepatocarcinogenesis. In 23 HBV-infected HCC clinical patient tumor and adjacent non-tumor control tissues, 17 and 19 tumors expressed HBx mRNA and protein, respectively. When considered as a group, HBV-infected HCC tumors had lower miR-338-3p expression than controls; however, miR-338-3p was only significantly down-regulated in HBx-positive tumors, indicating that HBx inversely correlated with miR-338-3p. Functional characterization of miR-338-3p indicated that miR-338-3p mimics inhibited cell proliferation by inducing cell cycle arrest at the G1/S phase as assessed by EdU and cell cycle assays in HBx-expressing LO2 cells. CyclinD1, containing two putative miR-338-3p targets, was confirmed as a direct target using 3'-UTR luciferase reporter assays from cells transfected with mutated binding sites. Mutating the 2397-2403 nt binding site conferred the greatest resistance to miR-338-3p suppression of CyclinD1, indicating that miR-338-3p suppresses CyclinD1 at this site. Overall, this study demonstrates that miR-338-3p inhibits proliferation by regulating CyclinD1, and HBx down-regulates miR-338-3p in HCC. This newly identified miR-338-3p/CyclinD1 interaction provides novel insights into HBx-mediated hepatocarcinogenesis and may facilitate therapeutic development against 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.