ArticleJournal of cellular and molecular medicine2017
Pleiotrophin, a target of miR-384, promotes proliferation, metastasis and lipogenesis in HBV-related hepatocellular carcinoma.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Pooled it
- Deletion of Pleiotrophin protects against high-fat diet-induced liver metabolic disease, independently of the sexual dimorphism in dietary response.Molecular biomedicine · 2026Article
- Cardiac PTN-SIRT1 axis alleviates oxidative stress and promotes mitochondrial energy reprogramming to mitigate doxorubicin-induced cardiotoxicity through AMPK/PGC1α signaling.Acta biochimica et biophysica Sinica · 2026Article
- In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma.Molecular oncology · 2026Article
- Clinical value of emerging peripheral blood protein biomarkers in prostate cancer (Review).Oncology letters · 2026Review
- The "viral-metabolic" interaction mechanisms and management challenges in chronic hepatitis B combined with metabolic dysfunction-associated fatty liver disease: from clinical evidence to an integrated multidisciplinary framework.Frontiers in immunology · 2026Review
- Liver-joint axis: Hepatitis B virus as a contributor to rheumatoid arthritis pathogenesis.Virulence · 2025Review
- Pleiotrophin modulates cell proliferation, prostate smooth muscle contraction and fibrosis in hyperplastic prostate.Journal of translational medicine · 2025Article
- Pleiotrophin promote glioma proliferation and invasion by enhancing NF-κB/SLUG mediated epithelial-mesenchymal transition.European journal of medical research · 2025Article
- The lncrna HMMR-AS1 promotes the malignant progression of ovarian cancer cells by regulating the miR-627-3p/PTN axis.Journal of ovarian research · 2025Article
- Unlocking the lipid code: SREBPs as key drivers in gastrointestinal tumour metabolism.Lipids in health and disease · 2025Review
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- MicroRNA-384 radiosensitizes human non-small cell lung cancer by impairing DNA damage response and repair signaling, which is inhibited by NF-κB.Cancer biology & medicine · 2024Article
- scRNA-Seq Analysis Revealed CAFs Regulating HCC Cells via PTN Signaling.Journal of hepatocellular carcinoma · 2024Article
- Dysregulated microRNAs as a biomarker for diagnosis and prognosis of hepatitis B virus-associated hepatocellular carcinoma.World journal of gastroenterology · 2023Review
- Single-cell RNA sequencing reveals the mediatory role of cancer-associated fibroblast PTN in hepatitis B virus cirrhosis-HCC progression.Gut pathogens · 2023Article
- Pleiotrophin and metabolic disorders: insights into its role in metabolism.Frontiers in endocrinology · 2023Review
- Key events in cancer: Dysregulation of SREBPs.Frontiers in pharmacology · 2023Review
- Article
- Serum proteomics links suppression of tumor immunity to ancestry and lethal prostate cancer.Nature communications · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) infection plays a crucial role and is a major cause of hepatocellular carcinoma (HCC) in China. microRNAs (miRNAs) have emerged as key players in hepatic steatosis and carcinogenesis. We found that down-regulation of miR-384 expression was a common event in HCC, especially HBV-related HCC. However, the possible function of miR-384 in HBV-related HCC remains unclear. The oncogene pleiotrophin (PTN) was a target of miR-384. HBx inhibited miR-384, increasing PTN expression. The PTN receptor N-syndecan was highly expressed in HCC. PTN induced by HBx acted as a growth factor via N-syndecan on hepatocytes and further promoted cell proliferation, metastasis and lipogenesis. PTN up-regulated sterol regulatory element-binding protein 1c (SREBP-1c) through the N-syndecan/PI3K/Akt/mTORC1 pathway and the expression of lipogenic genes, including fatty acid synthesis (FAS). PTN-mediated de novo lipid synthesis played an important role in HCC proliferation and metastasis. PI3K/AKT and an mTORC1 inhibitor diminished PTN-induced proliferation, metastasis and lipogenesis. Taken together, these data strongly suggest that the dysregulation of miR-384 could play a crucial role in HBV related to HCC, and the target gene of miR-384, PTN, represents a new potential therapeutic target for the prevention of hepatic steatosis and further progression to HCC after chronic HBV infection.
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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 Socratic graph.