ArticleBMC infectious diseases2021
Amygdalin promotes the activity of T cells to suppress the progression of HBV-related hepatocellular carcinoma via the JAK2/STAT3 signaling pathway.
Article in BMC infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Chinese medicine in the treatment of chronic hepatitis B: The mechanisms of signal pathway regulation.Heliyon · 2024Review
- Amygdalin as a Promising Anticancer Agent: Molecular Mechanisms and Future Perspectives for the Development of New Nanoformulations for Its Delivery.International journal of molecular sciences · 2023Review
- Xuanfei Baidu decoction in the treatment of coronavirus disease 2019 (COVID-19): Efficacy and potential mechanisms.Heliyon · 2023Review
- Long noncoding RNA regulatory factor X3- antisense RNA 1 promotes non-small cell lung cancer via the microRNA-577/signal transducer and activator of transcription 3 axis.Bioengineered · 2022Article
- A Risk Model Based on Sorafenib-Response Target Genes Predicts the Prognosis of Patients with HCC.Journal of oncology · 2022Article
- Synthesis, Characterization, and Antiproliferative Effect of CuO-TiOBioinorganic chemistry and applications · 2022Article
- Apoptosis-promoting properties of miR-3074-5p in MC3T3-E1 cells under iron overload conditions.Cellular & molecular biology letters · 2021Article
- Onco-immunity and therapeutic application of amygdalin: A review.Journal of oral biology and craniofacial researchReview
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHepatitis B virus (HBV) infection is a high-risk factor of hepatocellular carcinoma (HCC). Cellular immune responses are essential for HCC development, and the CD4+ and CD8+ T subtypes are identified as the primary anti-tumor immune cells. In the study, we investigated the effect and mechanism of amygdalin in the cellular immune response in HBV-related HCC and HCC progression.
methodsThe cell proliferation was examined by MTT analysis. Cells metastasis ability was detected by Invasion and migration assays. Quantification of apoptotic cells was performed with Flow cytometer assay. The protein levels of p-STAT3, STAT3, p-JAK2, JAK2, caspase-3, cleaved caspase-3 were detected by performing immunoblotting assays.
resultsWe demonstrate that amygdalin treatment could rescue the HBV-T cell viability and IFN-γ and TNF-αproduction. In HBV-T cells, the MFI levels of CD8
conclusionOur findings provide a rationale for further studies on the functions and mechanism of amygdalin inhibiting HBV-related HCC cell proliferation, invasion, and migration via T cell-mediated tumor immunity.
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Registered trials
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