Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway

Yuan, Chuanjian; Fan, Rong; Zhu, Kai; Wang, Yutong; Xie, Wenpeng; Liang, Yanchen

doi:10.1177/15353702231220670

Cited by 6 publications

(2 citation statements)

References 47 publications

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“…This effect can be reversed by the ferroptosis inhibitor Liproxstatin-1 (Lip-1) and the Nrf2 activator Bardoxolone methyl. 93 Additionally, the curcumin analog EF24 induces ferroptosis in OS cells by upregulating the expression of the ferroptosis-related gene HMOX1, without inducing other forms of cell death such as apoptosis, necroptosis, or autophagy. 92 The synthesis of AA is closely linked to the specific structural domain of ACSL3, and the splicing of ACSL3 pre-mRNA mediated by BRD4-SRPK2-SRSF2 enhances erastin-induced ferroptosis in OS cells.…”

Section: Drug-induced Ferroptosis In Osmentioning

confidence: 99%

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Ma,

Cong,

Shen

et al. 2024

Cell Biochemistry & Function

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Currently, challenges such as chemotherapy resistance, resulting from preoperative and postoperative chemotherapy, postoperative recurrence, and poor bone regeneration quality, are becoming increasingly prominent in osteosarcoma (OS) treatment. There is an urgent need to find more effective ways to address these issues. Ferroptosis is a novel form of iron‐dependent programmed cell death, distinct from other forms of cell death. In this paper, we summarize how, through the three major defense systems of ferroptosis, not only can substances from traditional Chinese medicine, antitumor drugs, and nano‐drug carriers induce ferroptosis in OS cells, but they can also be combined with immunotherapy, differentiation therapy, and other treatment modalities to significantly enhance chemotherapy sensitivity and inhibit tumor growth. Thus, ferroptosis holds great potential in treating OS, offering more choices and possibilities for future clinical interventions.

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Section: Drug-induced Ferroptosis In Osmentioning

confidence: 99%

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Ma,

Cong,

Shen

et al. 2024

Cell Biochemistry & Function

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“…Curcumin—This polyphenol derived from the turmeric rhizome of Curcuma longa L. is extensively described as an antitumor agent capable of constraining NF-κB pathway activation by interfering with IKK and blocking IκBα and p65 phosphorylation [ 305 ]. The literature reports numerous curcumin antiproliferative and antimigratory effects on OS with modulation of p21, Bax, Bcl-xl, Bcl2, caspase-3, PARP cleavage, cyclin D1, MMP-2, and MMP-9 expression [ 306 , 307 , 308 , 309 , 310 , 311 ].…”

Section: Experimental Evidence Nf-κb Inhibitionmentioning

confidence: 99%

Amicis Omnia Sunt Communia: NF-κB Inhibition as an Alternative to Overcome Osteosarcoma Heterogeneity

Medeiros,

Guenka,

Bastos

et al. 2024

Pharmaceuticals

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Tumor heterogeneity poses a significant challenge in osteosarcoma (OS) treatment. In this regard, the “omics” era has constantly expanded our understanding of biomarkers and altered signaling pathways (i.e., PI3K/AKT/mTOR, WNT/β-catenin, NOTCH, SHH/GLI, among others) involved in OS pathophysiology. Despite different players and complexities, many commonalities have been described, among which the nuclear factor kappa B (NF-κB) stands out. Its altered activation is pervasive in cancer, with pleiotropic action on many disease-relevant traits. Thus, in the scope of this article, we highlight the evidence of NF-κB dysregulation in OS and its integration with other cancer-related pathways while we summarize the repertoire of compounds that have been described to interfere with its action. In silico strategies were used to demonstrate that NF-κB is closely coordinated with other commonly dysregulated signaling pathways not only by functionally interacting with several of their members but also by actively participating in the regulation of their transcription. While existing inhibitors lack selectivity or act indirectly, the therapeutic potential of targeting NF-κB is indisputable, first for its multifunctionality on most cancer hallmarks, and secondly, because, as a common downstream effector of the many dysregulated pathways influencing OS aggressiveness, it turns complex regulatory networks into a simpler picture underneath molecular heterogeneity.

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Hyperoside induces ferroptosis in chronic myeloid leukemia cells by targeting NRF2

Wei,

Chai,

Qin

et al. 2024

Mol Med

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Background Hyperoside (quercetin-3-O-β-D-galactopyranoside) is a flavonol glycoside compound derived from plants in the Hypericum and Crataegus genera that reportedly exhibits an array of anti-inflammatory, antioxidant, and antitumor properties such that it has been used to treat various diseases. Whether it can serve as an effective treatment for chronic myeloid leukemia (CML) cells, however, has yet to be established. The present study was thus devised to assess the therapeutic effects of hyperoside on CML cells and to clarify the underlying mechanism of action. Methods Cellular viability, proliferative activity, migration, and apoptotic death were respectively analyzed through CCK-8, EDU, transwell, and flow cytometry assays. RNA-seq and bioinformatics approaches were further employed to evaluate the mechanisms through which hyperoside influences CML cells, while analyses of reactive oxygen species (ROS) and free iron were detected with commercial kits. Transmission electron microscopy was used to assess mitochondrial morphology. Molecular docking, cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) approaches were also used to explore the ability of hyperoside to target NRF2. Results From a mechanistic perspective, hyperoside was able to inhibit SLC7A11/GPX4 signaling in a manner that was abrogated by the ferroptosis inhibitor ferrostatin-1. NRF2 was also closely associated with the inactivation of the SLC7A11/GPX4 axis mediated by hyperoside such that overexpressing NRF2 ablated the benefits associated with hyperoside treatment. Conclusions The present analyses indicate that hyperoside can target the NRF2/SLC7A11/GPX4 axis to induce ferroptotic CML cell death.

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Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway

Cited by 6 publications

References 47 publications

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Amicis Omnia Sunt Communia: NF-κB Inhibition as an Alternative to Overcome Osteosarcoma Heterogeneity

Hyperoside induces ferroptosis in chronic myeloid leukemia cells by targeting NRF2

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