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Novel curcumin nanoformulation induces apoptosis, and reduces migration and angiogenesis in liver cancer cells. | LitMetric

AI Article Synopsis

  • Curcumin nanoparticles (Cur-NPs) were developed using PEG/chitosan to enhance the therapeutic effects of curcumin on liver cancer cells, which typically face limitations due to low pharmacologic profiles.
  • In tests, Cur-NPs showed cytotoxic effects on liver cancer cells (HepG2 and Huh 7) at concentrations as low as 6.25 µg/mL and inhibited cell migration significantly at higher doses.
  • The treatment led to decreased cell growth and induced apoptosis by altering the expression of critical proteins, promoting pro-apoptotic pathways while suppressing anti-apoptotic signals in liver cancer cells.

Article Abstract

Background: Curcumin has been used in the treatment of several diseases; however, its low pharmacologic profile reduces its therapeutic use. Towards improving its biological activity, nanoformulations have emerged. Thus, we aimed to determine whether curcumin nanoparticles (Cur-NPs) coated with PEG/chitosan improve the treatment of liver cancer (LC) cells and underpin the molecular mechanisms underlying their anti-cancer activity.

Methods: Cur-NPs were synthesised in the form of Cur-PLGA-PEG/chitosan NPs. The effect of Cur-NPs was assessed in HepG2 and Huh 7 LC cells and THLE-2 normal liver cells.

Results: The size of synthesised Cur-NPS was determined in the standard range of 141.2 ± 47.5 nm. Compared to THLE-2 cells, LC cells treated with Cur-NPs exerted cytotoxicity at 6.25 µg/mL after 48h. Treatment of HepG-2 cells with 2.5 µg/mL of Cur-NPs inhibited cell migration and this inhibition was augmented at 10 µg/mL ( < 0.001). Treatment of chicken embryo with 5 µg/mL Cur-NPs reduced angiogenesis ( < 0.001) of 4-day-old embryos. The nanoformulation upregulated Bax and p53 and downregulated Bcl-2 in a concentration-dependent manner and subsequently induce apoptosis in HepG-2 cells.

Conclusion: Treatment of LC cells with Cur-NPs decreased cell proliferation, migration, and angiogenesis, and induced cell death by promoting the proapoptotic pathway.

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Source
http://dx.doi.org/10.1080/21691401.2023.2238756DOI Listing

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