Novel perspective in pancreatic cancer therapy: Targeting ferroptosis pathway DOI Open Access
Yang Yang, Zijian Zhang, Yu Wen

et al.

World Journal of Gastrointestinal Oncology, Journal Year: 2021, Volume and Issue: 13(11), P. 1668 - 1679

Published: Nov. 12, 2021

Pancreatic cancer is a highly lethal malignancy with low resection and survival rates not sensitive to radiotherapy chemotherapy. Ferroptosis novel form of nonapoptotic regulated cell death characterized by the accumulation lipid peroxides reactive oxygen species involved in iron metabolism. has significant role occurrence development various tumors. Previous studies have shown that regulating ferroptosis-induced inhibited tumor growth pancreatic was synergistic other antitumor drugs improve treatment sensitivity. Herein, we discuss mechanism, inducers, developments ferroptosis provide new strategies for malignancy.

Language: Английский

A guideline on the molecular ecosystem regulating ferroptosis DOI
Enyong Dai, Xin Chen, Andreas Linkermann

et al.

Nature Cell Biology, Journal Year: 2024, Volume and Issue: 26(9), P. 1447 - 1457

Published: Feb. 29, 2024

Language: Английский

Citations

77
Ferroptosis: principles and significance in health and disease DOI Creative Commons
Fangquan Chen, Rui Kang, Daolin Tang

et al.

Journal of Hematology & Oncology, Journal Year: 2024, Volume and Issue: 17(1)

Published: June 6, 2024

Abstract Ferroptosis, an iron-dependent form of cell death characterized by uncontrolled lipid peroxidation, is governed molecular networks involving diverse molecules and organelles. Since its recognition as a non-apoptotic pathway in 2012, ferroptosis has emerged crucial mechanism numerous physiological pathological contexts, leading to significant therapeutic advancements across wide range diseases. This review summarizes the fundamental mechanisms regulatory pathways underlying ferroptosis, including both GPX4-dependent -independent antioxidant mechanisms. Additionally, we examine involvement various conditions, cancer, neurodegenerative diseases, sepsis, ischemia–reperfusion injury, autoimmune disorders, metabolic disorders. Specifically, explore role response chemotherapy, radiotherapy, immunotherapy, nanotherapy, targeted therapy. Furthermore, discuss pharmacological strategies for modulating potential biomarkers monitoring this process. Lastly, elucidate interplay between other forms regulated death. Such insights hold promise advancing our understanding context human health disease.

Language: Английский

Citations

52
Cellular metabolism: A key player in cancer ferroptosis DOI Creative Commons

Xianjie Jiang,

Qiu Peng,

Mingjing Peng

et al.

Cancer Communications, Journal Year: 2024, Volume and Issue: 44(2), P. 185 - 204

Published: Jan. 13, 2024

Abstract Cellular metabolism is the fundamental process by which cells maintain growth and self‐renewal. It produces energy, furnishes raw materials, intermediates for biomolecule synthesis, modulates enzyme activity to sustain normal cellular functions. foundation of life processes plays a regulatory role in various biological functions, including programmed cell death. Ferroptosis recently discovered form iron‐dependent The inhibition ferroptosis crucial tumorigenesis tumor progression. However, metabolism, particularly glucose amino acid cancer not well understood. Here, we reviewed glucose, lipid, acid, iron selenium involvement elucidate impact different metabolic pathways on this process. Additionally, provided detailed overview agents used induce ferroptosis. We explained that maintaining intracellular redox homeostasis disrupting these renders them more susceptible iron‐induced death, resulting enhanced killing. combination inducers inhibitors may be novel approach future therapy an important strategy advance development treatments.

Language: Английский

Citations

23
Impact of polystyrene microplastics with combined contamination of norfloxacin and sulfadiazine on Chrysanthemum coronarium L. DOI Open Access
Kiran Yasmin Khan, Guanlin Li, Daolin Du

et al.

Environmental Pollution, Journal Year: 2022, Volume and Issue: 316, P. 120522 - 120522

Published: Oct. 26, 2022

Language: Английский

Citations

39
The bioengineered and multifunctional nanoparticles in pancreatic cancer therapy: Bioresponisive nanostructures, phototherapy and targeted drug delivery DOI Open Access
Mohamed J. Saadh,

Hala Baher,

Yuanji Li

et al.

Environmental Research, Journal Year: 2023, Volume and Issue: 233, P. 116490 - 116490

Published: June 22, 2023

Language: Английский

Citations

32
Ferroptosis in gastrointestinal cancer: from mechanisms to implications DOI Creative Commons
Ruoxi Zhang, Rui Kang, Daolin Tang

et al.

Cancer Letters, Journal Year: 2023, Volume and Issue: 561, P. 216147 - 216147

Published: March 24, 2023

Language: Английский

Citations

26
Molecular Classification of Breast Cancer Utilizing Long Non-Coding RNA (lncRNA) Transcriptomes Identifies Novel Diagnostic lncRNA Panel for Triple-Negative Breast Cancer DOI Open Access
Hibah Shaath, Ramesh Elango, Nehad M. Alajez

et al.

Cancers, Journal Year: 2021, Volume and Issue: 13(21), P. 5350 - 5350

Published: Oct. 26, 2021

Breast cancer remains the world's most prevalent cancer, responsible for around 685,000 deaths globally despite international research efforts and advances in clinical management. While estrogen receptor positive (ER+), progesterone (PR+), human epidermal growth factor (HER2+) subtypes are easily classified can be targeted, there no direct diagnostic test triple-negative breast (TNBC), except lack of receptors expression. The identification long non-coding RNAs (lncRNAs) roles they play progression has recently proven to beneficial. In current study, we utilize RNA sequencing data identify lncRNA-based biomarkers associated with TNBC, ER+ subtypes, normal tissue. Marker Finder algorithm identified lncRNA transcript panel each molecular subtype receiver operating characteristic (ROC) analysis was used validate potential (area under curve (AUC) ≥8.0 p value < 0.0001). Focusing on findings from discovery cohort were validated an additional two cohorts, identifying 13 common transcripts enriched TNBC. Binary regression a four signature (ENST00000425820.1, ENST00000448208.5, ENST00000521666.1, ENST00000650510.1) highest power ENST00000671612.1 correlated worse refractory free survival (RFS). Our provides step towards finding novel TNBC therapeutic implications.

Language: Английский

Citations

43
CD4 T cell-secreted IFN-γ in Sjögren's syndrome induces salivary gland epithelial cell ferroptosis DOI Creative Commons

Jiannan Zhou,

Janak L. Pathak,

Tingting Cao

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2024, Volume and Issue: 1870(4), P. 167121 - 167121

Published: March 11, 2024

Language: Английский

Citations

8
Formins in Human Disease DOI Creative Commons
Leticia Labat-de-Hoz, Miguel A. Alonso

Cells, Journal Year: 2021, Volume and Issue: 10(10), P. 2554 - 2554

Published: Sept. 27, 2021

Almost 25 years have passed since a mutation of formin gene, DIAPH1, was identified as being responsible for human inherited disorder: form sensorineural hearing loss. Since then, our knowledge the links between formins and disease has deepened considerably. Mutations DIAPH1 six other genes (DAAM2, DIAPH2, DIAPH3, FMN2, INF2 FHOD3) been genetic cause variety disorders, including intellectual disability, renal disease, peripheral neuropathy, thrombocytopenia, primary ovarian insufficiency, loss cardiomyopathy. In addition, alterations in associated with pathological conditions, developmental defects affecting heart, nervous system kidney, aging-related diseases, cancer. This review summarizes most recent discoveries about involvement monogenic disorders especially cancer, which they associated. vitro results experiments modified animal models are discussed. Finally, we outline directions future research this field.

Language: Английский

Citations

36
ROS Induction Targets Persister Cancer Cells with Low Metabolic Activity in NRAS-Mutated Melanoma DOI Creative Commons
Ossia M. Eichhoff, Corinne I. Stoffel, Jan Käsler

et al.

Cancer Research, Journal Year: 2023, Volume and Issue: 83(7), P. 1128 - 1146

Published: March 22, 2023

Abstract Clinical management of melanomas with NRAS mutations is challenging. Targeting MAPK signaling only beneficial to a small subset patients due resistance that arises through genetic, transcriptional, and metabolic adaptation. Identification targetable vulnerabilities in NRAS-mutated melanoma could help improve patient treatment. Here, we used multiomics analyses reveal cells adopt mesenchymal phenotype quiescent program resist cellular stress induced by MEK inhibition. The alterations elevated baseline reactive oxygen species (ROS) levels, leading these become highly sensitive ROS induction. In vivo xenograft experiments single-cell RNA sequencing demonstrated intratumor heterogeneity necessitates the combination inducer inhibitor inhibit both tumor growth metastasis. Ex pharmacoscopy 62 human metastatic confirmed inhibitor–resistant tumors significantly benefited from therapy. Finally, oxidative response translational suppression corresponded ROS-inducer sensitivity 486 cancer cell lines, independent type. These findings link transcriptional plasticity can be inhibited inducers other cancers. Significance: Metabolic reprogramming drug-resistant confers induction, which suppresses metastasis pathway inhibitors.

Language: Английский

Citations

14