Prunus Armeniaca L. Seed Extract and Its Amygdalin Containing Fraction Induced Mitochondrial-Mediated Apoptosis and Autophagy in Liver Carcinogenesis

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Author(s): Samar Hosny, Heba Sahyon, Magdy Youssef, Amr Negm*

Journal Name: Anti-Cancer Agents in Medicinal Chemistry
(Formerly Current Medicinal Chemistry - Anti-Cancer Agents)

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Background: Despite significant advances in therapeutic interventions, liver cancer is the leading cause of cancer mortality in the world. Potential phytochemicals have shown to be promising agents against many life-threatening diseases because of their low toxicity and potential effectiveness.

Objective: The current study aims to an in vitro investigation of the anticancer activity of Apricot Extract (AE) and Amygdalin Containing Fraction (ACF), additionally studying their therapeutic effects in DMBA-induced liver carcinogenesis mice model to highlight their related biochemical and molecular mechanisms.

Methods and Results: Amygdalin was isolated from the seeds of P. armeniaca L. Male mice received AE or ACF, DMBA, DMBA+AE, DMBA+ACF, and vehicles. The oxidative stress and antioxidant markers, cell proliferation by flow cytometric analysis of Proliferating Cell Nuclear Antigen (PCNA) expression, angiogenesis marker (VEGF), inflammatory marker (TNF-α), apoptotic, anti-apoptotic and autophagy genes expression (caspase-3, Bcl-2, and Beclin-1) were investigated.AE and ACF were found to stimulate the apoptotic process by up-regulating caspase-3 expression and down-regulating Bcl-2 expression. They also reduce VEGF and PCNA levels and increasing the antioxidant defense system. Moreover, AE and ACF treatments also inhibit HepG2 and EAC cell proliferation and up-regulate Beclin-1 expression.

Conclusion: This study provides evidence that, in DMBA-induced hepatocarcinogenesis, the key proteins involved in the proliferation, angiogenesis, autophagy, and apoptosis are feasible molecular targets for hepatothrapeutic potential using AE and ACF.

Keywords: Amygdalin, Bcl-2, beclin-1, caspase-3, hepatocarcinogenesis, autophagy

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(E-pub Ahead of Print)
DOI: 10.2174/1871520620666200608124003
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