Bavachin Induces Ferroptosis through the STAT3/P53/SLC7A11 Axis in Osteosarcoma Cells

Luo, Yi; Gao, Xu; Zou, Luetao; Miao, Lei; Jiang, Feng; Hu, Zhenming

doi:10.1155/2021/1783485

Cited by 86 publications

(66 citation statements)

References 50 publications

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“…As displayed in Figure 3C , the expression of SLC7A11 in the Nano-PEG@CeO 2 group was significantly downregulated, in comparison with the control group. It was reflected that Nano-PEG@CeO 2 could regulate ferroptosis of tumor cells, as similarly reported before ( Hong et al, 2021 ; Luo et al, 2021b ). Furthermore, the expression of p53 with Nano-PMI@CeO 2 treatment was remarkably increased compared with the control group.…”

Section: Resultssupporting

confidence: 80%

Assembling p53 Activating Peptide With CeO2 Nanoparticle to Construct a Metallo-Organic Supermolecule Toward the Synergistic Ferroptosis of Tumor

Wang

He²,

Zhang³

et al. 2022

Front. Bioeng. Biotechnol.

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Inducing lipid peroxidation and subsequent ferroptosis in cancer cells provides a potential approach for anticancer therapy. However, the clinical translation of such therapeutic agents is often hampered by ferroptosis resistance and acquired drug tolerance in host cells. Emerging nanoplatform-based cascade engineering and ferroptosis sensitization by p53 provides a viable rescue strategy. Herein, a metallo-organic supramolecular (Nano-PMI@CeO2) toward p53 restoration and subsequent synergistic ferroptosis is constructed, in which the radical generating module-CeO2 nanoparticles act as the core, and p53-activator peptide (PMI)-gold precursor polymer is in situ reduced and assembled on the CeO2 surface as the shell. As expected, Nano-PMI@CeO2 effectively reactivated the p53 signaling pathway in vitro and in vivo, thereby downregulating its downstream gene GPX4. As a result, Nano-PMI@CeO2 significantly inhibited tumor progression in the lung cancer allograft model through p53 restoration and sensitized ferroptosis, while maintaining favorable biosafety. Collectively, this work develops a tumor therapeutic with dual functions of inducing ferroptosis and activating p53, demonstrating a potentially viable therapeutic paradigm for sensitizing ferroptosis via p53 activation. It also suggests that metallo-organic supramolecule holds great promise in transforming nanomedicine and treating human diseases.

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Section: Resultssupporting

confidence: 80%

Assembling p53 Activating Peptide With CeO2 Nanoparticle to Construct a Metallo-Organic Supermolecule Toward the Synergistic Ferroptosis of Tumor

Wang

He²,

Zhang³

et al. 2022

Front. Bioeng. Biotechnol.

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“…SLC7A11 and GPX4 may be the most valuable pharmacological targets in the ferroptosis network. This has been confirmed by several studies on traditional antitumors drugs such as olaparib ( Hong et al, 2021 ), tanshinone IIA ( Guan et al, 2020 ) and bavachin ( Luo et al, 2021 ). The poly (ADP-ribose) polymerase olaparib has been demonstrated to promote ferroptosis in ovarian cancer cells by downregulating SLC7A11 expression ( Hong et al, 2021 ).…”

Section: Effects Of P53 Ptms On Ferroptosismentioning

confidence: 54%

“…Tanshinone IIA, the active ingredient of Chinese herbal medicine Salvia miltiorrhiza Bunge, also promotes ferroptosis in gastric cancer cells via p53/SLC7A11 ( Guan et al, 2020 ). Bavachin induces ferroptosis in osteosarcoma cells via repressing SLC7A11 ( Luo et al, 2021 ). Interestingly, bavachin also increases intracellular labile iron levels ( Luo et al, 2021 ).…”

Section: Effects Of P53 Ptms On Ferroptosismentioning

confidence: 99%

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Post-Translational Modifications of p53 in Ferroptosis: Novel Pharmacological Targets for Cancer Therapy

et al. 2022

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The tumor suppressor p53 is a well-known cellular guardian of genomic integrity that blocks cell cycle progression or induces apoptosis upon exposure to cellular stresses. However, it is unclear how the remaining activities of p53 are regulated after the abrogation of these routine activities. Ferroptosis is a form of iron- and lipid-peroxide-mediated cell death; it is particularly important in p53-mediated carcinogenesis and corresponding cancer prevention. Post-translational modifications have clear impacts on the tumor suppressor function of p53. Here, we review the roles of post-translational modifications in p53-mediated ferroptosis, which promotes the elimination of tumor cells. A thorough understanding of the p53 functional network will be extremely useful in future strategies to identify pharmacological targets for cancer therapy.

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“…This finding suggested that STAT3 is a risk gene in gliomas, consistent with the results of the present study 36 . Hu et al found that bavachin could induce ferroptosis through the STAT3/P53/SLC7A11 Axis 37 . Furthermore, CA9 was shown to be highly overexpressed in GBM, conferring radiation resistance in glioma cells 38 , 39 .…”

Section: Discussionmentioning

confidence: 99%

Construction of a novel radiosensitivity- and ferroptosis-associated gene signature for prognosis prediction in gliomas

Xie¹,

Xiao²,

Liu³

et al. 2022

J. Cancer

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Background: Gliomas are the most refractory intracranial disease characterized by high incidence and mortality rates. Therefore, radiotherapy plays a crucial role in the treatment of gliomas. However, recent evidence reveals that ferroptosis is highly associated with radiosensitivity in tumor cells. Therefore, this study aimed to investigate radiosensitivity- and ferroptosis-associated biomarkers. Moreover, the study aimed to provide new strategies for the treatment and evaluation of prognosis in gliomas. Methods: The mRNA sequencing and relevant clinical data were obtained from The Cancer Genome Atlas (TCGA). Secondly, differential analysis was conducted to reveal the radiosensitivity- and ferroptosis-associated differentially expressed genes (DEGs). Further, a predictive model based on the seven genes was constructed, and LASSO regression analysis was carried out. After that, the Chinese Glioma Genome Atlas (CGGA) was used for validation of the results. Results: A total of 36 radiosensitivity- and 19 ferroptosis-associated DEGs with a prognostic value were identified. Moreover, seven intersecting genes (HSPB1, STAT3, CA9, MAP1LC3A, MAPK1, ZEB1, and TNFAIP3) were identified as the risk signature genes. The ROC curves and K-M analysis revealed that the signature genes showed a good survival prediction. Furthermore, the functional analysis revealed that the differentially expressed genes between the high-risk and the low-risk groups were enriched in glioma-related biological processes. In addition, differences were reported in immune function status between the two groups. Conclusion: This study revealed that the seven biomarkers could help predict the prognosis in glioma patients. In addition, this study provides a basis for understanding the molecular mechanisms of radiosensitivity and ferroptosis in the treatment of gliomas.

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Bavachin Induces Ferroptosis through the STAT3/P53/SLC7A11 Axis in Osteosarcoma Cells

Cited by 86 publications

References 50 publications

Assembling p53 Activating Peptide With CeO2 Nanoparticle to Construct a Metallo-Organic Supermolecule Toward the Synergistic Ferroptosis of Tumor

Assembling p53 Activating Peptide With CeO2 Nanoparticle to Construct a Metallo-Organic Supermolecule Toward the Synergistic Ferroptosis of Tumor

Post-Translational Modifications of p53 in Ferroptosis: Novel Pharmacological Targets for Cancer Therapy

Construction of a novel radiosensitivity- and ferroptosis-associated gene signature for prognosis prediction in gliomas

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