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Applications of Antiviral Nanoparticles in Cancer Therapy
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
Anusha Konatala, Sai Brahma Penugonda, Fain Parackel, Sudhakar Pola
In a fascinating study conducted by Ou et al. (2017), low density lipoprotein NPs were conjugated with docosahexaenoic acid (LDL-DHA), and their anticancer activity was measured. They described a novel anti-apoptotic iron-mediated cell-death pathway called ferroptosis, caused by the LDL-DHA AVNPs through which rat and human HCC cell lines were killed. Three features that stood out in this cell-death pathway were the lipid peroxidation, depletion of glutathione, and the inactivation of the lipid antioxidant glutathione peroxidase (GPX4). In an extension of their in vitro study, the group also studied the in vivo effect of LDL-DHA on tumour xenografts in mice and found that the intratumoral injections inhibited the growth of HCC long-term and caused ferroptic cell death. In a study to understand the therapeutic potential of, and to create an efficient delivery system for, umbelliferone β-D-galactopyranoside (UFG), Wistar rats with diethyl nitrosamine (DEN)-induced HCC were investigated in vivo, and HuH-7 and Hep-G2 were investigated in vitro. The group experimented with a PLGA NP-based delivery system prepared and loaded with UFG through sonication. DEN-induced reactive oxygen species generation, mitochondrial dysfunction, and pro-inflammatory cytokine alteration were used to characterise the anticancer potential of UFG-PLGA-NPs. In a similar study by a group of researchers, rutin-loaded PLGA NPs were assessed for their anticancer activity in in vitro, in vivo, and biochemical studies. They found that the RT-PLGA-NPs administered orally reduced the incidence of hepatic nodules and exhibited significant anticancer activity.
miR-761-hepcidin/Gpx4 pathway contribute to unexplained liver dysfunction in polycystic ovary syndrome by regulating liver iron overload and ferroptosis
Published in Gynecological Endocrinology, 2023
Ruoheng Zheng, Chuanping Lin, Yuchan Mao, Fan Jin
The phenomenon of chronic inflammation and Fe changes within PCOS patients lead us think whether the liver damage of PCOS may be related to ferroptosis which is a new type of programmed cell death with Fe dependent and different from apoptosis, necrosis and autophagy. The main mechanism of ferroptosis relies on the action of divalent Fe and lipoxygenase. In detail, unsaturated fatty acids that are highly expressed on cell membrane are catalyzed to produce lipid peroxidation, thus inducing cell death. GPX4-mediated neutralization of lipid peroxidation, cellular lipid peroxide levels can be enzymatically enhanced by lipoxygenases. Thus, lipoxygenase and GPX4 have opposite functions in ferroptosis: lipoxygenase causes the formation of lipid peroxides, while GPX4 eliminates them. In addition, GPX4, the core enzyme of antioxidant system (glutathione system) [30] and marker of ferroptosis was decreased in our study.
Ferritinophagy was involved in long-term SiNPs exposure induced ferroptosis and liver fibrosis
Published in Nanotoxicology, 2023
Qingqing Liang, Yuexiao Ma, Fenghong Wang, Mengqi Sun, Lisen Lin, Tianyu Li, Junchao Duan, Zhiwei Sun
Glutathione peroxidase 4 (GPX4) is an enzyme that effectively reduced the toxic lipid peroxides to nontoxic phosphatidyl alcohols using two molecules of the reduced glutathione with sulfhydryl group (GSH). The Cyclooxygenase-2 (COX-2) was a marker of lipid peroxidation. Western blot was used to detect the GPX4 and COX-2 expression levels in liver tissues of rats after long-term SiNPs exposure or exposure cessation and recovery, to characterize SiNPs-induced ferroptosis in hepatocytes. The data revealed that GPX4 and COX-2 were clearly down-regulated and up-regulated, respectively, in the long-term SiNPs exposure group compared with the corresponding control group (p<0.05). However, no significant difference in the expression of GPX4 and COX-2 was detected in the liver tissues of rats after exposure cessation and recovery (p>0.05) (Figure 2(E,F,G)).
Red ginseng polysaccharide exhibits anticancer activity through GPX4 downregulation-induced ferroptosis
Published in Pharmaceutical Biology, 2022
Feng-guo Zhai, Qi-chao Liang, Yi-yan Wu, Jia-qi Liu, Jia-wei Liu
Considering the essential role of GPX4 in ferroptosis, we therefore assessed the effects of RGP treatment on GPX4 expression. Interestingly, we found that RGP treatment downregulated GPX4 expression and demonstrated that GPX4 overexpression conferred drug resistance. We therefore propose that targeting GPX4 is a promising therapeutic approach in the treatment of lung and breast cancers. Importantly, it was the first time to illustrated the role of RGP in the ferroptosis in lung or breast cancer cells. Moreover, RGP suppressed the progression of lung or breast cancer cells that might target GPX4. Our findings not only enhanced the understating into the effects of RGP in the progression of lung and breast cancer cells but also provided evidence to indicate its potential role in developing the therapy for patient with lung or breast cancer.