Ferroptosis suppressed the growth of melanoma that may be related to DNA damage

Wang, Zhenying; Jin, Di; Ma, Dongmei; Ji, Cancan; Wu, Wenxian; Xu, Linlin; Zhang, Li

doi:10.1111/dth.12921

Cited by 10 publications

(8 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, Fe-MBG can kill cancer cells through the release of iron ions which would lead to intracellular Fenton’s reaction, producing ROS and ultimately induce tumor cell ferroptosis ( Figure 7 ). Along with this, it has recently been reported that ferroptosis can suppress the growth of melanoma and may thus serve as a new treatment target for the research and development of drugs and/or treatment regimens [ 143 ]. Finally, ferroptosis-inducing drugs can also be loaded into Fe-MBG and provide synergism with the iron ions release.…”

Section: Mbgs For Skin Cancer Therapymentioning

confidence: 99%

Mesoporous Silica Nanoparticles and Mesoporous Bioactive Glasses for Wound Management: From Skin Regeneration to Cancer Therapy

et al. 2021

View full text Add to dashboard Cite

Exploring new therapies for managing skin wounds is under progress and, in this regard, mesoporous silica nanoparticles (MSNs) and mesoporous bioactive glasses (MBGs) offer great opportunities in treating acute, chronic, and malignant wounds. In general, therapeutic effectiveness of both MSNs and MBGs in different formulations (fine powder, fibers, composites etc.) has been proved over all the four stages of normal wound healing including hemostasis, inflammation, proliferation, and remodeling. The main merits of these porous substances can be summarized as their excellent biocompatibility and the ability of loading and delivering a wide range of both hydrophobic and hydrophilic bioactive molecules and chemicals. In addition, doping with inorganic elements (e.g., Cu, Ga, and Ta) into MSNs and MBGs structure is a feasible and practical approach to prepare customized materials for improved skin regeneration. Nowadays, MSNs and MBGs could be utilized in the concept of targeted therapy of skin malignancies (e.g., melanoma) by grafting of specific ligands. Since potential effects of various parameters including the chemical composition, particle size/morphology, textural properties, and surface chemistry should be comprehensively determined via cellular in vitro and in vivo assays, it seems still too early to draw a conclusion on ultimate efficacy of MSNs and MBGs in skin regeneration. In this regard, there are some concerns over the final fate of MSNs and MBGs in the wound site plus optimal dosages for achieving the best outcomes that deserve careful investigation in the future.

show abstract

Section: Mbgs For Skin Cancer Therapymentioning

confidence: 99%

Mesoporous Silica Nanoparticles and Mesoporous Bioactive Glasses for Wound Management: From Skin Regeneration to Cancer Therapy

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In melanoma, withstanding oxidative stress accompanying transient metabolic alterations has been recognized as a determinant of successful metastasis [181], suggesting that sensitivity of melanoma cells to ferroptosis may vary during melanoma development and progression. It has also been suggested that ferroptosis may be triggered upon DNA damage in melanoma cells [182]. In addition, several oncogenic pathways relevant for melanoma have been The disturbances in the synthesis of glutathione can be associated with inhibition of the cystine/glutamate antiporter named system X C − , which is composed of the twelve-pass transmembrane protein solute carrier family 7 member 11 (SLC7A11; xCT, light chain) connected to a single-pass transmembrane regulatory protein SLC3A2 (4F2, heavy chain) [13].…”

Section: Ferroptosis In Melanomamentioning

confidence: 99%

“…In melanoma, withstanding oxidative stress accompanying transient metabolic alterations has been recognized as a determinant of successful metastasis [181], suggesting that sensitivity of melanoma cells to ferroptosis may vary during melanoma development and progression. It has also been suggested that ferroptosis may be triggered upon DNA damage in melanoma cells [182]. In addition, several oncogenic pathways relevant for melanoma have been shown to render cancer cells susceptible to ferroptosis via the modulation of essential regulators of this type of cell death.…”

Section: Ferroptosis In Melanomamentioning

confidence: 99%

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Hartman

2020

IJMS

View full text Add to dashboard Cite

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAF mut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

show abstract

“…Ferroptosis, a type of programmed cell death characterized by the accumulation of reactive oxygen species caused by iron accumulation and lipid peroxidation (7), have been proved to be different from apoptosis, necroptosis and pyroptosis (8). Ferroptosis affects cell proliferation, metastasis, and immune response in cancers.…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis-related lncRNA signature predicts prognosis and immunotherapy efficacy in cutaneous melanoma

Niu

Yang

et al. 2022

Front. Surg.

View full text Add to dashboard Cite

PurposeFerroptosis-related lncRNAs are promising biomarkers for predicting the prognosis of many cancers. However, a ferroptosis-related signature to predict the prognosis of cutaneous melanoma (CM) has not been identified. The purpose of this study was to construct a ferroptosis-related lncRNA signature to predict prognosis and immunotherapy efficacy in CM.MethodsFerroptosis-related differentially expressed genes (FDEGs) and lncRNAs (FDELs) were identified using TCGA, GTEx, and FerrDb datasets. We performed Cox and LASSO regressions to identify key FDELs, and constructed a risk score to stratify patients into high- and low-risk groups. The lncRNA signature was evaluated using the areas under the receiver operating characteristic curves (AUCs) and Kaplan-Meier analyses in the training, testing, and entire cohorts. Multivariate Cox regression analyses including the lncRNA signature and common clinicopathological characteristics were performed to identify independent predictors of overall survival (OS). A nomogram was developed for clinical use. We performed gene set enrichment analyses (GSEA) to identify significantly enriched pathways. Differences in the tumor microenvironment (TME) between the 2 groups were assessed using 7 algorithms. To predict the efficacy of immune checkpoint inhibitors (ICI), we analyzed the association between PD1 and CTLA4 expression and the risk score. Finally, differences in Tumor Mutational Burden (TMB) and molecular drugs Sensitivity between the 2 groups were performed.ResultsWe identified 5 lncRNAs (AATBC, AC145423.2, LINC01871, AC125807.2, and AC245041.1) to construct the risk score. The AUC of the lncRNA signature was 0.743 in the training cohort and was validated in the testing and entire cohorts. Kaplan-Meier analyses revealed that the high-risk group had poorer prognosis. Multivariate Cox regression showed that the lncRNA signature was an independent predictor of OS with higher accuracy than traditional clinicopathological features. The 1-, 3-, and 5-year survival probabilities for CM patients were 92.7%, 57.2%, and 40.2% with an AUC of 0.804, indicating a good accuracy and reliability of the nomogram. GSEA showed that the high-risk group had lower ferroptosis and immune response. TME analyses confirmed that the high-risk group had lower immune cell infiltration (e.g., CD8+ T cells, CD4+ memory-activated T cells, and M1 macrophages) and lower immune functions (e.g., immune checkpoint activation). Low-risk patients whose disease expressed PD1 or CTLA4 were likely to respond better to ICIs. The analysis demonstrated that the TMB had significantly difference between low- and high- risk groups. Chemotherapy drugs, such as sorafenib, Imatinib, ABT.888 (Veliparib), Docetaxel, and Paclitaxel showed Significant differences in the estimated IC50 between the two risk groups.ConclusionOur novel ferroptosis-related lncRNA signature was able to accurately predict the prognosis and ICI outcomes of CM patients. These ferroptosis-related lncRNAs might be potential biomarkers and therapeutic targets for CM.

show abstract

Ferroptosis suppressed the growth of melanoma that may be related to DNA damage

Cited by 10 publications

References 29 publications

Mesoporous Silica Nanoparticles and Mesoporous Bioactive Glasses for Wound Management: From Skin Regeneration to Cancer Therapy

Mesoporous Silica Nanoparticles and Mesoporous Bioactive Glasses for Wound Management: From Skin Regeneration to Cancer Therapy

Non-Apoptotic Cell Death Signaling Pathways in Melanoma

Ferroptosis-related lncRNA signature predicts prognosis and immunotherapy efficacy in cutaneous melanoma

Contact Info

Product

Resources

About