ArticleYonsei medical journal2020
MicroRNA-98-5p Inhibits Tumorigenesis of Hepatitis B Virus-Related Hepatocellular Carcinoma by Targeting NF-κB-Inducing Kinase.
Article in Yonsei medical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Nanocarrier-mediated targeting of NF-κB and JAK/STAT signaling pathways in hepatocellular carcinoma: mechanisms and therapeutic strategies.Journal of experimental & clinical cancer research : CR · 2026Review
- Predictive value and mechanism of LINC00665 for liver dysfunction in pregnant women with hepatitis B during early pregnancy.Virology journal · 2026Article
- Multi-omics profiling identifies ESM1 as a key mediator of immunoevasion through the SPP1 pathway in bladder cancer.Scientific reports · 2025Article
- MiR-362-3p mediates IFNα-induced antiviral viability against Enterovirus 71 (EV71).Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- A comprehensive overview on the crosstalk between microRNAs and viral pathogenesis and infection.Medicinal research reviews · 2025Review
- Identification of novel microRNAs: Biomarkers for pathogenesis of hepatocellular carcinoma in mice model.Biochemistry and biophysics reports · 2025Article
- Non-coding RNAs as key regulators in hepatitis B virus-related hepatocellular carcinoma.Frontiers in immunology · 2025Review
- MicroRNA-98: the multifaceted regulator in human cancer progression and therapy.Cancer cell international · 2024Review
- Serum microRNA Profiles and Pathways in Hepatitis B-Associated Hepatocellular Carcinoma: A South African Study.International journal of molecular sciences · 2024Review
- Differentially expressed non-coding RNAs and their regulatory networks in liver cancer.Heliyon · 2023Review
- mir-98-5p regulates gluconeogenesis and lipogenesis by targeting PPP1R15B in hepatocytes.Journal of cell communication and signaling · 2023Article
- Non-coding RNA in SARS-CoV-2: Progress toward therapeutic significance.International journal of biological macromolecules · 2022Review
- Progress and Prospects of Non-Canonical NF-κB Signaling Pathway in the Regulation of Liver Diseases.Molecules (Basel, Switzerland) · 2022Review
- The Therapeutic Potential of Targeting NIK in B Cell Malignancies.Frontiers in immunology · 2022Review
- Noncanonical NF-κB Signaling Pathway in Liver Diseases.Journal of clinical and translational hepatology · 2021Review
- The Crosstalk Between Regulatory Non-Coding RNAs and Nuclear Factor Kappa B in Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMicroRNAs play key regulatory roles in the tumorigenesis of hepatitis B virus-related hepatocellular carcinoma (HBV-HCC). This study aimed to explore the regulatory effects of microRNA-98-5p (miR-98-5p) on the proliferation, migration, invasion, and apoptosis of HBV-HCC cells, as well as the underlying mechanisms involving nuclear factor-κB-inducing kinase (NIK). MATERIALS AND
methodsThe expressions of miR-98-5p and NIK in HBV-HCC tissues and cells, and the level of HBV DNA in HBV-HCC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration, invasion, and apoptosis of HBV-HCC cells were analyzed by cell counting kit-8, wound healing, transwell, and flow cytometry assay, respectively. The targeting relationship between miR-98-5p and NIK was predicted by StarBase3.0 and verified by dual-luciferase reporter assay. HBV-HCC xenograft tumor model was constructed in mice to observe the tumor growth in vivo.
resultsThe expression of miR-98-5p was declined in HBV-HCC tissues and cells. Overexpression of miR-98-5p markedly reduced the level of HBV DNA; inhibited the proliferation, migration, and invasion; and promoted the apoptosis of HBV-HCC cells. NIK was a target of miR-98-5p. Overexpression of miR-98-5p markedly decreased the protein expression of NIK in MHCC97H-HBV cells. NIK reversed the tumor-suppressing effect of miR-98-5p on HBV-HCC cells. Furthermore, overexpression of miR-98-5p significantly inhibited the xenograft tumor growth and decreased the expression of NIK in mice.
conclusionMiR-98-5p inhibits the secretion of HBV, proliferation, migration, and invasion of HBV-HCC cells by targeting NIK.
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