Xanthatin inhibits non‐small cell lung cancer proliferation by breaking the redox balance

Xie, Yanbo; Zhu, Xiaodong; Liu, Ping; Liu, Yunxiao; Geng, Yadi; Zhang, Lei

doi:10.1002/ddr.21941

Cited by 10 publications

(5 citation statements)

References 35 publications

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“…In the following study, they found that xanthatin ( 1 ) could suppress DNA replication by triggering Chk1-mediated DNA damage [ 71 ]. In 2018, Fang et al, reported that xanthatin ( 1 ) could promote the oxidative stress-mediated apoptosis of HeLa cells via inhibiting thioredoxin reductase, which was supported by the research of Zhang et al, in 2021 [ 72 , 73 ]. In 2019, Yu et al, demonstrated that xanthatin could covalently bind to JAK and IKK kinases and inhibit the STAT3 and NF-κB signalling pathways to suppress the development of cancer and inflammatory diseases [ 74 ].…”

Section: The Biological Activity Of Xanthanolidesmentioning

confidence: 90%

Xanthanolides in Xanthium L.: Structures, Synthesis and Bioactivity

et al. 2022

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Xanthanolides were particularly characteristic of the genus Xanthium, which exhibited broad biological effects and have drawn much attention in pharmacological application. The review surveyed the structures and bioactivities of the xanthanolides in the genus Xanthium, and summarized the synthesis tactics of xanthanolides. The results indicated that over 30 naturally occurring xanthanolides have been isolated from the genus Xanthium in monomeric, dimeric and trimeric forms. The bioassay-guided fractionation studies suggested that the effective fractions on antitumor activities were mostly from weak polar solvents, and xanthatin (1) was the most effective and well-studied xanthanolide. The varieties of structures and structure-activity relationships of the xanthanolides had provided the promising skeleton for the further study. The review aimed at providing guidance for the efficient preparation and the potential prospects of the xanthanolides in the medicinal industry.

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Section: The Biological Activity Of Xanthanolidesmentioning

confidence: 90%

Xanthanolides in Xanthium L.: Structures, Synthesis and Bioactivity

et al. 2022

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“…For example, Verma et al found that isodeoxyelephantopin and deoxyelephantopin can inhibit the activation of NF-κB by inducing the production of ROS and inhibit the growth of breast cancer [ 55 ]. Xanthatin, a sesquiterpenoid derived from Xanthium strumarium L, may induce the elevation of ROS, mitochondrial injury, and apoptosis in non-small cell lung cancer (NSCLC) [ 56 ]. The ability of sesquiterpenes to induce ROS generation may stem from the fact that they both have α-methylene-γ-lactone and [ 57 ] a cyclopentenone ring-like structure (butenolide in scabertopin) ( Figure 1 A) [ 58 ].…”

Section: Discussionmentioning

confidence: 99%

Scabertopin Derived from Elephantopus scaber L. Mediates Necroptosis by Inducing Reactive Oxygen Species Production in Bladder Cancer In Vitro

Gao

Nie

Cao

et al. 2022

Cancers

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Bladder cancer remains one of the most common malignant tumors that threatens human health worldwide. It imposes a heavy burden on patients and society due to the high medical costs associated with its easy metastasis and recurrence. Although several treatment options for bladder cancer are available, their clinical efficacy remains unsatisfactory. Therefore, actively exploring new drugs and their mechanisms of action for the clinical treatment of bladder cancer is very important. Scabertopin is one of the major sesquiterpene lactones found in Elephantopus scaber L. Sesquiterpene lactones are thought to have fairly strong anti-cancer efficacy. However, the anticancer effect of sesquiterpenoid scabertopin on bladder cancer and its mechanism are still unclear. The aim of this study is to evaluate the antitumor activity of scabertopin in bladder cancer and its potential molecular mechanism in vitro. Our results suggest that scabertopin can induce RIP1/RIP3-dependent necroptosis in bladder cancer cells by promoting the production of mitochondrial reactive oxygen species (ROS), inhibit the expression of MMP-9 by inhibiting the FAK/PI3K/Akt signaling pathway, and ultimately inhibit the migration and invasion ability of bladder cancer cells. At the same time, we also demonstrated that the half-inhibition concentration (IC50) of scabertopin on various bladder cancer cell lines (J82, T24, RT4 and 5637) is much lower than that on human ureteral epithelial immortalized cells (SV-HUC-1). The above observations indicate that scabertopin is a potential therapeutic agent for bladder cancer that acts by inducing necroptosis and inhibiting metastasis.

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“…High-dose NAC inhalation therapy shows promise in rectifying the oxidant-antioxidant imbalance observed in lung tissue of IPF patients, thereby ameliorating fibrotic progression [ 180 ]. β-mercaptoethanol functions as a reducing agent that facilitates cysteine uptake for maintaining optimal GSH levels [ 181 , 182 ]. Studies have demonstrated that β-mercaptoethanol can inhibit the proliferation of human lung fibroblasts by modulating ferroptosis-related pathway [ 183 ].…”

Section: Strategies For Targeted Ferroptosis In Pfmentioning

confidence: 99%

Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges

Hu,

Huang,

Zong

et al. 2024

Cell Death Discov.

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Pulmonary fibrosis (PF) is a chronic interstitial lung disorder characterized by abnormal myofibroblast activation, accumulation of extracellular matrix (ECM), and thickening of fibrotic alveolar walls, resulting in deteriorated lung function. PF is initiated by dysregulated wound healing processes triggered by factors such as excessive inflammation, oxidative stress, and coronavirus disease (COVID-19). Despite advancements in understanding the disease’s pathogenesis, effective preventive and therapeutic interventions are currently lacking. Ferroptosis, an iron-dependent regulated cell death (RCD) mechanism involving lipid peroxidation and glutathione (GSH) depletion, exhibits unique features distinct from other RCD forms (e.g., apoptosis, necrosis, and pyroptosis). Imbalance between reactive oxygen species (ROS) production and detoxification leads to ferroptosis, causing cellular dysfunction through lipid peroxidation, protein modifications, and DNA damage. Emerging evidence points to the crucial role of ferroptosis in PF progression, driving macrophage polarization, fibroblast proliferation, and ECM deposition, ultimately contributing to alveolar cell death and lung tissue scarring. This review provides a comprehensive overview of the latest findings on the involvement and signaling mechanisms of ferroptosis in PF pathogenesis, emphasizing potential novel anti-fibrotic therapeutic approaches targeting ferroptosis for PF management.

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Xanthatin inhibits non‐small cell lung cancer proliferation by breaking the redox balance

Cited by 10 publications

References 35 publications

Xanthanolides in Xanthium L.: Structures, Synthesis and Bioactivity

Xanthanolides in Xanthium L.: Structures, Synthesis and Bioactivity

Scabertopin Derived from Elephantopus scaber L. Mediates Necroptosis by Inducing Reactive Oxygen Species Production in Bladder Cancer In Vitro

Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges

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