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Investigation of folate-modified EGCG-loaded thermosensitive nanospheres inducing immunogenic cell death and damage-associated molecular patterns in hepatocellular carcinoma. | LitMetric

AI Article Synopsis

  • The study addresses a challenge in treating advanced hepatocellular carcinoma and explores the anti-tumor effects of EGCG, a compound from green tea, particularly its ability to induce immunogenic cell death (ICD).
  • Researchers created a nano-drug delivery system for EGCG and tested its effects on HepG2 cells, finding that it significantly reduced cell viability, migration, and invasion while also inducing apoptosis through various assays.
  • Results showed that EGCG not only decreased HepG2 cell survival in a dose-dependent manner but also increased the expression of damage-associated molecular patterns (DAMPs), confirming its potential use in cancer treatment.

Article Abstract

Background: The systemic treatment of advanced hepatocellular carcinoma is currently facing a bottleneck. EGCG, the primary active compound in green tea, exhibits anti-tumor effects through various pathways. However, there is a lack of study on EGCG-induced immunogenic cell death (ICD) in hepatocellular carcinoma.

Methods: In a previous study, we successfully synthesized folate-modified thermosensitive nano-materials, encapsulated EGCG within nanoparticles using a hydration method, and established the EGCG nano-drug delivery system. The viability of HepG2 cells post-EGCG treatment was assessed via the MTT and EdU assays. Cell migration and invasion were evaluated through wound healing experiments, Transwell assays, and Annexin V-FITC/PI assay for apoptosis detection. Additionally, the expression levels of damage-associated molecular patterns (DAMPs) were determined using immunofluorescence, ATP measurement, RT-qPCR, and Western Blot.

Results: The drug sensitivity test revealed an IC50 value of 96.94 μg/mL for EGCG in HepG2 cells after 48 h. EGCG at a low concentration (50 μg/mL) significantly impeded the migration and invasion of HepG2 cells, showing a clear dose-dependent response. Moreover, medium to high EGCG concentrations induced cell apoptosis in a dose-dependent manner and upregulated DAMPs expression. Immunofluorescence analysis demonstrated a notable increase in CRT expression following low-concentration EGCG treatment. As EGCG concentration increased, cell viability decreased, leading to CRT exposure on the cell membrane. EGCG also notably elevated ATP levels. RT-qPCR and Western Blot analyses indicated elevated expression levels of HGMB1, HSP70, and HSP90 following EGCG intervention.

Conclusion: EGCG not only hinders the proliferation, migration, and invasion of hepatocellular carcinoma cells and induces apoptosis, but also holds significant clinical promise in the treatment of malignant tumors by promoting ICD and DAMPs secretion.

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Source
http://dx.doi.org/10.1016/j.bbrc.2024.149976DOI Listing

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