Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells

Li, Ruihua; Zhang, Jing; Zhou, Yongfeng; Gao, Qi; Wang, Rui; Fu, Yurong; Zheng, Lianwen; Yu, Hao

doi:10.1155/2020/3469840

Cited by 96 publications

(79 citation statements)

References 54 publications

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“…Curcumin is a yellow polyphenol compound derived from the turmeric plant, which shows anticancer properties through a variety of mechanisms, including inhibition of tumor proliferation, invasion and metastases, regulation of apoptosis, and autophagy 8 . Recent studies showed that curcumin can treat glioblastoma and breast cancer via regulating ferroptosis 9,10 . However, there seem to be few studies exploring the relationship of ferroptosis and anti‐NSCLC induced by curcumin.…”

Section: Introductionmentioning

confidence: 99%

Curcumin induces ferroptosis in non‐small‐cell lung cancer via activating autophagy

et al. 2021

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Background Emerging studies showed curcumin can inhibit glioblastoma and breast cancer cells via regulating ferroptosis. However, the role of ferroptosis in the inhibitory effect of curcumin on non‐small‐cell lung cancer (NSCLC) remains unclear. Methods Cell counting kit‐8 (CCK‐8) assay was used to measure the viability of A549 and H1299 cells under different conditions. Cell proliferation was examined by Ki67 immunofluorescence. The morphological changes of cells and tumor tissues were observed by optical microscope and hematoxylin and eosin (H&E) staining. Intracellular reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and iron contents were determined by corresponding assay kit. The related protein expression levels were detected by western blot and immunohistochemistry. Transmission electron microscope was used to observe ultrastructure changes of A549 and H1299 cells. Results Curcumin inhibited tumor growth and cell proliferation, but promoted cell death. Characteristic changes of ferroptosis were observed in curcumin group, including iron overload, GSH depletion and lipid peroxidation. Meanwhile, the protein level of ACSL4 was higher and the levels of SLC7A11 and GPX4 were lower in curcumin group than that in control group. Incubation of ferroptosis inhibitors ferrostatin‐1 (Fer‐1) or knockdown of iron‐responsive element‐binding protein 2 (IREB2) notably weakened curcumin‐induced anti‐tumor effect and ferroptosis in A549 and H1299 cells. Further investigation suggested that curcumin induced mitochondrial membrane rupture and mitochondrial cristae decrease, increased autolysosome, increased the level of Beclin1 and LC3, and decreased the level of P62. Curcumin‐induced autophagy and subsequent ferroptosis were both alleviated with autophagy inhibitor chloroquine (CQ) or siBeclin1. Conclusion Curcumin induced ferroptosis via activating autophagy in NSCLC, which enhanced the therapeutic effect of NSCLC.

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Section: Introductionmentioning

confidence: 99%

Curcumin induces ferroptosis in non‐small‐cell lung cancer via activating autophagy

et al. 2021

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“…Curcumin (CUR) has been widely and safely consumed as a natural food coloring for hundreds of years, and there have been a large number of studies showing its antioxidant, anticancer and anti-inflammatory properties [ 15 , 16 ]. Curcumin can not only effectively remove reactive oxygen species, but also activate antioxidant response elements to inhibit oxidative stress induced by reactive oxygen species [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Alleviates LPS-Induced Oxidative Stress, Inflammation and Apoptosis in Bovine Mammary Epithelial Cells via the NFE2L2 Signaling Pathway

Fang

Shen

et al. 2021

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Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. The purpose of this study is to investigate whether CUR can reduce the damage of bovine mammary epithelial cells (MAC-T) induced by LPS and its underlying molecular mechanism. The MAC-T cell line was treated with different concentrations of LPS and CUR for 24 h. The results showed that CUR rescued the decrease of MAC-T cell viability and cell damage induced by LPS. At the same time, 10 µM CUR and 100 µg/mL LPS were used to treat the cells in the follow-up study. The results showed CUR treatment reduced the accumulation of reactive oxygen species (ROS), the expression of inflammatory cytokines (tumor necrosis factor-a (TNF-α), interleukin-8 (IL-8), IL-6 and IL-1β) and the rate of apoptosis induced by LPS. These effects were associated with the activation of the nuclear factor E2-related factor 2 (NFE2L2)-antioxidant response element (ARE) pathway coupled with inactivation of the nuclear factor-κB (NF-κB) inflammatory and caspase/Bcl2 apoptotic pathways.

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“…Proteins involved in iron metabolism, such as transferrin, transferrin receptor 1, and ferroportin, as well as HO-1, have been implicated in the ferroptotic process [ 80 , 91 , 92 ]. Transcriptome Investigation by Li et al, highlighted the role of HO-1 in curcumin-induced ferroptosis [ 93 ].…”

Section: Ho-1 and Ferroptosismentioning

confidence: 99%

Heme Oxygenase-1 Signaling and Redox Homeostasis in Physiopathological Conditions

et al. 2021

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Heme-oxygenase is the enzyme responsible for degradation of endogenous iron protoporphyirin heme; it catalyzes the reaction’s rate-limiting step, resulting in the release of carbon monoxide (CO), ferrous ions, and biliverdin (BV), which is successively reduced in bilirubin (BR) by biliverdin reductase. Several studies have drawn attention to the controversial role of HO-1, the enzyme inducible isoform, pointing out its implications in cancer and other diseases development, but also underlining the importance of its antioxidant activity. The contribution of HO-1 in redox homeostasis leads to a relevant decrease in cells oxidative damage, which can be reconducted to its cytoprotective effects explicated alongside other endogenous mechanisms involving genes like TIGAR (TP53-induced glycolysis and apoptosis regulator), but also to the therapeutic functions of heme main transformation products, especially carbon monoxide (CO), which has been shown to be effective on GSH levels implementation sustaining body’s antioxidant response to oxidative stress. The aim of this review was to collect most of the knowledge on HO-1 from literature, analyzing different perspectives to try and put forward a hypothesis on revealing yet unknown HO-1-involved pathways that could be useful to promote development of new therapeutical strategies, and lay the foundation for further investigation to fully understand this important antioxidant system.

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Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells

Cited by 96 publications

References 54 publications

Curcumin induces ferroptosis in non‐small‐cell lung cancer via activating autophagy

Curcumin induces ferroptosis in non‐small‐cell lung cancer via activating autophagy

Curcumin Alleviates LPS-Induced Oxidative Stress, Inflammation and Apoptosis in Bovine Mammary Epithelial Cells via the NFE2L2 Signaling Pathway

Heme Oxygenase-1 Signaling and Redox Homeostasis in Physiopathological Conditions

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