Laminarin from Seaweed (Laminaria japonica) Inhibits Hepatocellular Carcinoma Through Upregulating Senescence Marker Protein-30
Autor: | Guo-Rong Luo, Yan-Fei Li, Lin Tian, Fa-Rong Mo, Tian-Ming Huang, Nai-Xia Chao, Chun-Mei Li |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Senescence Cancer Research Carcinoma Hepatocellular proliferation 03 medical and health sciences Laminarin chemistry.chemical_compound Mice 0302 clinical medicine Algae SENESCENCE MARKER PROTEIN 30 medicine Animals Humans Radiology Nuclear Medicine and imaging Glucans antitumor Cell Proliferation Pharmacology biology Liver Neoplasms apoptosis Intracellular Signaling Peptides and Proteins food and beverages General Medicine Original Articles hepatocellular carcinoma senescence marker protein-30 biology.organism_classification medicine.disease Seaweed Xenograft Model Antitumor Assays digestive system diseases 030104 developmental biology Oncology chemistry Apoptosis 030220 oncology & carcinogenesis Hepatocellular carcinoma Cancer research Laminaria japonica laminarin |
Zdroj: | Cancer Biotherapy & Radiopharmaceuticals |
ISSN: | 1557-8852 1084-9785 |
Popis: | Objective: This study aimed at investigating the specific roles of laminarin from seaweed (Laminaria japonica) in hepatocellular carcinoma (HCC) and its potential mechanisms related to senescence marker protein-30 (SMP-30). Materials and Methods: Human HCC cell lines, including Bel-7404 and HepG2, were incubated with different concentrations of laminarin (0, 5, 15, 25, 35, and 45 mg/mL). The cell viability and apoptosis rates were detected by WST-8 cell proliferation assay and flow cytometry, respectively. Hepa 1–6 tumor-bearing mice were injected with different concentrations of laminarin (400, 800, and 1200 mg/kg·d), and tumor volume and weight were measured. The expression of SMP-30 was detected in laminarin-treated Bel-7404 and HepG2 HCC cells and LO2 normal liver cells by quantitative real-time PCR and Western blotting. Results: The treatment with laminarin (48 h) significantly decreased the viability and increased the apoptosis rates of Bel-7404 and HepG2 cells in a dose-dependent manner. The injection of laminarin also significantly decreased the tumor volumes (beginning on the 10th day) and tumor weights (30 d post-injection) of mice in a dose-dependent manner. In addition, the treatment with laminarin (35 mg/mL for 48 h) significantly upregulated SMP-30 in Bel-7404 and HepG2 cells but not in LO2 cells. Conclusion: Laminarin inhibited the proliferation of Bel-7404 and HepG2 cells and inhibited the growth of tumors in Hepa 1–6 tumor-bearing mice by upregulating SMP-30. |
Databáze: | OpenAIRE |
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