Abstract:Ferroptosis is a distinct form of cell death mechanism different from the traditional ones. Ferroptosis is characterized biochemically by lipid peroxidation, iron accumulation, and glutathione deficiency. It has already demonstrated significant promise in antitumor therapy. Cervical cancer (CC) progression is closely linked to iron regulation and oxidative stress. Existing research has investigated the role of ferroptosis in CC. Ferroptosis could open up a new avenue of research for treating CC. This review wi… Show more
“… 57 Ferroptosis also plays an important role in the malignant biological behaviour and treatment of cervical cancer. 26 circLMO1 suppresses cervical cancer growth and metastasis via ferroptosis. 58 Ferroptosis, which is regulated by the Cdc25A/PKM2/ErbB2 pathway, may serve as a therapeutic target in cervical cancer.…”
Section: Discussionmentioning
confidence: 99%
“… 25 Furthermore, ferroptosis is involved in the occurrence and development of cervical cancer and is related to its prognosis. 26 , 27 , 28 , 29 , 30 Some drugs exert therapeutic effects against cervical cancer through ferroptosis. 31 , 32 , 33 Hypoxia reduces Fenton chemistry and lipoxygenase activity, which are the key control systems for ferroptosis.…”
Hypoxia and Ferroptosis are associated with the malignant behaviour of cervical cancer. Endothelial PAS domain‐containing protein 1 (EPAS1) contributes to the progression of cervical cancer. EPAS1 plays important roles in hypoxia and ferroptosis. Using the GEO dataset, machine‐learning algorithms were used to screen for hypoxia‐ and ferroptosis‐related genes (HFRGs) in cervical cancer. EPAS1 was identified as the hub gene. qPCR and WB were used to investigate the expression of EPAS1 in normal and cervical cancer tissues. The proliferation, invasion and migration of EPAS1 cells in HeLa and SiHa cell lines were detected using CCK8, transwell and wound healing assays, respectively. Apoptosis was detected by flow cytometry. A dual‐luciferase assay was used to analyse the MALAT1‐miR‐182‐5P‐EPAS1 mRNA axis and core promoter elements of the super‐enhancer. EPAS1 was significantly overexpressed in cervical cancer tissues. EPAS1 could increase the proliferation, invasion, migration of HeLa and SiHa cells and reduce the apoptosis of HeLa and SiHa cell. According to the double‐luciferase assay, EPAS1 expression was regulated by the MALAT1‐Mir‐182‐5p‐EPAS1 mRNA axis. EPAS1 is associated with super‐enhancers. Double‐luciferase assay showed that the core elements of the super‐enhancer were E1 and E3. EPAS1, an HFRG, is significantly overexpressed in cervical cancer. EPAS1 promotes malignant behaviour of cervical cancer cells. EPAS1 expression is regulated by super‐enhancers and the MALAT1‐miR‐182‐5P‐ EPAS1 mRNA axis. EPAS1 may be a target for the diagnosis and treatment of cervical cancer.
“… 57 Ferroptosis also plays an important role in the malignant biological behaviour and treatment of cervical cancer. 26 circLMO1 suppresses cervical cancer growth and metastasis via ferroptosis. 58 Ferroptosis, which is regulated by the Cdc25A/PKM2/ErbB2 pathway, may serve as a therapeutic target in cervical cancer.…”
Section: Discussionmentioning
confidence: 99%
“… 25 Furthermore, ferroptosis is involved in the occurrence and development of cervical cancer and is related to its prognosis. 26 , 27 , 28 , 29 , 30 Some drugs exert therapeutic effects against cervical cancer through ferroptosis. 31 , 32 , 33 Hypoxia reduces Fenton chemistry and lipoxygenase activity, which are the key control systems for ferroptosis.…”
Hypoxia and Ferroptosis are associated with the malignant behaviour of cervical cancer. Endothelial PAS domain‐containing protein 1 (EPAS1) contributes to the progression of cervical cancer. EPAS1 plays important roles in hypoxia and ferroptosis. Using the GEO dataset, machine‐learning algorithms were used to screen for hypoxia‐ and ferroptosis‐related genes (HFRGs) in cervical cancer. EPAS1 was identified as the hub gene. qPCR and WB were used to investigate the expression of EPAS1 in normal and cervical cancer tissues. The proliferation, invasion and migration of EPAS1 cells in HeLa and SiHa cell lines were detected using CCK8, transwell and wound healing assays, respectively. Apoptosis was detected by flow cytometry. A dual‐luciferase assay was used to analyse the MALAT1‐miR‐182‐5P‐EPAS1 mRNA axis and core promoter elements of the super‐enhancer. EPAS1 was significantly overexpressed in cervical cancer tissues. EPAS1 could increase the proliferation, invasion, migration of HeLa and SiHa cells and reduce the apoptosis of HeLa and SiHa cell. According to the double‐luciferase assay, EPAS1 expression was regulated by the MALAT1‐Mir‐182‐5p‐EPAS1 mRNA axis. EPAS1 is associated with super‐enhancers. Double‐luciferase assay showed that the core elements of the super‐enhancer were E1 and E3. EPAS1, an HFRG, is significantly overexpressed in cervical cancer. EPAS1 promotes malignant behaviour of cervical cancer cells. EPAS1 expression is regulated by super‐enhancers and the MALAT1‐miR‐182‐5P‐ EPAS1 mRNA axis. EPAS1 may be a target for the diagnosis and treatment of cervical cancer.
The supply and control of iron is essential for all cells and vital for many physiological processes. All functions and activities of iron are expressed in conjunction with iron-binding molecules. For example, natural chelators such as transferrin and chelator–iron complexes such as haem play major roles in iron metabolism and human physiology. Similarly, the mainstay treatments of the most common diseases of iron metabolism, namely iron deficiency anaemia and iron overload, involve many iron–chelator complexes and the iron-chelating drugs deferiprone (L1), deferoxamine (DF) and deferasirox. Endogenous chelators such as citric acid and glutathione and exogenous chelators such as ascorbic acid also play important roles in iron metabolism and iron homeostasis. Recent advances in the treatment of iron deficiency anaemia with effective iron complexes such as the ferric iron tri-maltol complex (feraccru or accrufer) and the effective treatment of transfusional iron overload using L1 and L1/DF combinations have decreased associated mortality and morbidity and also improved the quality of life of millions of patients. Many other chelating drugs such as ciclopirox, dexrazoxane and EDTA are used daily by millions of patients in other diseases. Similarly, many other drugs or their metabolites with iron-chelation capacity such as hydroxyurea, tetracyclines, anthracyclines and aspirin, as well as dietary molecules such as gallic acid, caffeic acid, quercetin, ellagic acid, maltol and many other phytochelators, are known to interact with iron and affect iron metabolism and related diseases. Different interactions are also observed in the presence of essential, xenobiotic, diagnostic and theranostic metal ions competing with iron. Clinical trials using L1 in Parkinson’s, Alzheimer’s and other neurodegenerative diseases, as well as HIV and other infections, cancer, diabetic nephropathy and anaemia of inflammation, highlight the importance of chelation therapy in many other clinical conditions. The proposed use of iron chelators for modulating ferroptosis signifies a new era in the design of new therapeutic chelation strategies in many other diseases. The introduction of artificial intelligence guidance for optimal chelation therapeutic outcomes in personalised medicine is expected to increase further the impact of chelation in medicine, as well as the survival and quality of life of millions of patients with iron metabolic disorders and also other diseases.
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