Next Article in Journal
Current and Emerging Methods of Antibiotic Susceptibility Testing
Previous Article in Journal
Health Predictors of Pain in Elderly—A Serbian Population-Based Study
Article Menu

Export Article

Open AccessArticle

HAMP Downregulation Contributes to Aggressive Hepatocellular Carcinoma via Mechanism Mediated by Cyclin4-Dependent Kinase-1/STAT3 Pathway

1,2,3,†, 1,2,3,†, 1,2,3, 1,3, 1,2,3, 1,2,3 and 1,3,*
1
Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen 518057, China
2
School of Life Science, Northwestern Polytechnical University, Xi’an 710072, China
3
Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environment Biophysics, School of Life Science, Northwestern Polytechnical University, Xi’an 710072, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Diagnostics 2019, 9(2), 48; https://doi.org/10.3390/diagnostics9020048
Received: 24 April 2019 / Accepted: 28 April 2019 / Published: 30 April 2019
(This article belongs to the Section Pathology and Molecular Diagnostics)
  |  
PDF [6470 KB, uploaded 30 April 2019]
  |  

Abstract

Background: Hepcidin encoded by HAMP is vital to regulating proliferation, metastasis, and migration. Hepcidin is secreted specifically by the liver. This study sought to examine the functional role of hepcidin in hepatocellular carcinoma (HCC). Methods: Data in the Cancer Genome Atlas database was used to analyze HAMP expression as it relates to HCC prognosis. We then used the 5-ethynyl-20-deoxyuridine (EdU) incorporation assay, transwell assay, and flow cytometric analysis, respectively, to assess proliferation, migration, and the cell cycle. Gene set enrichment analysis (GSEA) was used to find pathways affected by HAMP. Results: HAMP expression was lower in hepatocellular carcinoma samples compared with adjacent normal tissue controls. Low HAMP expression was linked with a higher rate of metastasis and poor disease-free status. Downregulation of HAMP induced SMMC-7721 and HepG-2 cell proliferation and promoted their migration. HAMP could affect the cell cycle pathway and Western blotting, confirming that reduced HAMP levels activated cyclin-dependent kinase-1/stat 3 pathway. Conclusion: Our findings indicate that HAMP functions as a tumor suppressor gene. The role of HAMP in cellular proliferation and metastasis is related to cell cycle checkpoints. HAMP could be considered as a diagnostic biomarker and targeted therapy in HCC. View Full-Text
Keywords: hepatocellular carcinoma; HAMP; metastasis; cell cycle; iron hepatocellular carcinoma; HAMP; metastasis; cell cycle; iron
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Shen, Y.; Li, X.; Su, Y.; Badshah, S.A.; Zhang, B.; Xue, Y.; Shang, P. HAMP Downregulation Contributes to Aggressive Hepatocellular Carcinoma via Mechanism Mediated by Cyclin4-Dependent Kinase-1/STAT3 Pathway. Diagnostics 2019, 9, 48.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Diagnostics EISSN 2075-4418 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top