Lipid metabolism and oxidative stress in HPV-related cancers

Cruz-Gregorio, Alfredo; Aranda-Rivera, Ana Karina; Ortega-Lozano, Ariadna Jazmín; Pedraza‐Chaverrí, José; Mendoza-Hoffmann, Francisco

doi:10.1016/j.freeradbiomed.2021.06.009

Cited by 25 publications

(17 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…OS causes lipids, proteins, or nucleic acids oxidation. The latter leads to cellular processes such as apoptosis, necrosis, or cancer 16,25,26 . OS might participate in cancer development by triggering genotoxic (direct DNA damage) and nongenotoxic (epigenetic and cell signaling alterations) mechanisms 27 …”

Section: Os and Redox‐sensitive Signaling Pathways In Cancermentioning

confidence: 99%

Redox‐sensitive signaling pathways in renal cell carcinoma

et al. 2021

Self Cite

View full text Add to dashboard Cite

Renal cell carcinoma (RCC) is one of the most lethal urological cancers, highly resistant to chemo and radiotherapy. Obesity and smoking are the best-known risk factors of RCC, both related to oxidative stress presence, suggesting a significant role in RCC development and maintenance. Surgical resection is the treatment of choice for localized RCC; however, this neoplasia is hardly diagnosable at its initial stages, occurring commonly in late phases and even when metastasis is already present. Systemic therapies are the option against RCC in these more advanced stages, such as cytokine therapy or a combination of tyrosine kinase inhibitors with immunotherapies; nevertheless, these strategies are still insufficient. A field poorly analyzed in this neoplasia is the status of cell

show abstract

Section: Os and Redox‐sensitive Signaling Pathways In Cancermentioning

confidence: 99%

Redox‐sensitive signaling pathways in renal cell carcinoma

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…The incubation with LPS resulted in the decrease in expression of GPX4 in VECs ( Figure 2A and B ). Furthermore, the metabolomics analysis in hierarchical clustering heatmap and chord plot showed that the biosynthesis of unsaturated fatty acids such as arachidonic acid was significantly increased after sepsis, which was an important factor leading to ferroptosis 28 ( Figure 2C and D , Supplementary Figure 1 ). The lipid peroxidation levels were enhanced in the LPS-stimulated VECs ( Figure 2E and F ), and the MDA levels of superior mesenteric vein tissues in septic rats also increased by 82% ( Figure 2G ).…”

Section: Resultsmentioning

confidence: 99%

Protective Effects of Dexmedetomidine on Sepsis-Induced Vascular Leakage by Alleviating Ferroptosis via Regulating Metabolic Reprogramming

She¹,

Hu²,

Zhou³

et al. 2021

JIR

View full text Add to dashboard Cite

Introduction Vascular leakage plays a vital role in sepsis-induced multi-organ dysfunction. Currently, no specific measures are available for vascular leakage. Ferroptosis, as a recently recognized form of cell death, plays a crucial role in cell dysfunction. It is still unknown whether ferroptosis participates in the occurrence of organ dysfunction following sepsis. Our previous study showed that dexmedetomidine (Dex) could alleviate sepsis-induced organ dysfunction. However, whether the mechanism is related to ferroptosis is not clear. Methods The publicly available datasets of septic patients were reanalyzed, and septic models in vivo and vitro by cecal ligation and puncture and lipopolysaccharide-stimulated vascular endothelial cells (VECs) were applied. The occurrence of ferroptosis in septic patients and rats was observed, and the protective effects of Dex on ferroptosis, and related mechanisms on regulating metabolic reprogramming and mitochondrial fission were further studied. Results The transcriptomics data of patients from the GEO database showed that ferroptosis was closely related to sepsis. Sepsis induced significant ferroptosis in VECs by metabolomics analysis. The level of lipid peroxidation was increased in VECs, and the mitochondrial cristae was decreased after sepsis. Metabolomics analysis showed that Dex activated the pentose phosphate pathway and increased glutathione in VECs via up-regulation of G6PD expression. Dex could antagonize sepsis-induced the decrease in the level of Nrf2. The Nrf2 inhibitor reversed the protective effect of Dex on ferroptosis. Further study showed that Dex significantly alleviated sepsis-induced mitochondrial over-division, improved mitochondrial function, and decreased ROS, further inhibiting the ferroptosis of VECs. Dex alleviated the permeability of vessels by reducing ferroptosis and enhanced the intercellular junction of VECs. Conclusion Dex protects vascular leakage following sepsis by inhibiting ferroptosis. The mechanism is mainly related to metabolic reprogramming via Nrf2 up-regulation and inhibition of mitochondrial fission.

show abstract

“…HPV infection leads to a series of changes in cell proliferation, cell death evasion, and genomic instability by influencing lipid metabolism and oxidative stress and thereby determines cell fate [ 12 ]. It was reported that HPV-positive cervical cancer cells presented metabolic reprogramming by promoting SIRT expression [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that inducing ferroptosis by inhibiting intracellular GPX4 is a potential approach for the treatment of cancers in women [ 11 ]. Ferroptosis was recently reported to have dual functions: ferroptosis acts not only as a defense mechanism, but can also promote oncogenesis [ 12 , 13 ]. HPV-related cancer cells have the ability to counteract lipid peroxidation [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Persistent ferroptosis promotes cervical squamous intraepithelial lesion development and oncogenesis by regulating KRAS expression in patients with high risk-HPV infection

et al. 2022

View full text Add to dashboard Cite

Cervical squamous cell carcinoma (CSCC) is a type of female cancer that affects millions of families worldwide. Human papillomavirus (HPV) infection is the main reason for CSCC formation, and squamous intraepithelial lesions (SILs) induced by high-risk HPV (HR-HPV) infection are considered precancerous lesions. A previous study reported that HPV-infected cancer cells were able to counteract lipid peroxidation for survival. Recent research has reported that ferroptosis acts in an iron-dependent lipid peroxidation manner to kill cancer cells, and it is proposed as a new approach for female cancer therapy. Here, we investigated the role of ferroptosis throughout SIL development into CSCC. We found that ferroptosis occurred in SIL, but anti-ferroptosis emerged in CSCC. Our data further indicated that an antiferroptotic effect was formed in response to persistent ferroptosis and then promoted oncogenesis. Altogether, we provide novel insight into ferroptosis in cervical SIL development and suggest a potential therapeutic target for the treatment of CSCC.

show abstract

Lipid metabolism and oxidative stress in HPV-related cancers

Cited by 25 publications

References 101 publications

Redox‐sensitive signaling pathways in renal cell carcinoma

Redox‐sensitive signaling pathways in renal cell carcinoma

Protective Effects of Dexmedetomidine on Sepsis-Induced Vascular Leakage by Alleviating Ferroptosis via Regulating Metabolic Reprogramming

Persistent ferroptosis promotes cervical squamous intraepithelial lesion development and oncogenesis by regulating KRAS expression in patients with high risk-HPV infection

Contact Info

Product

Resources

About