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Your search keyword '"chromatin remodeling factor"' showing total 3 results
Start Over Descriptor "chromatin remodeling factor" Journal molecular cancer
3 results on '"chromatin remodeling factor"'

1. The epigenetic regulators and metabolic changes in ferroptosis-associated cancer progression

Author

Yuqing Wu, Siwei Zhang, Xiaoxiao Gong, Samantha Tam, Desheng Xiao, Shuang Liu, and Yongguang Tao

Subjects
Ferroptosis, Epigenetics, Cancer, Organelles, Chromatin remodeling factor, lncRNA, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Ferroptosis, a novel form of regulated cell death, is different from other types of cell death in morphology, genetics and biochemistry. Increasing evidence indicates that ferroptosis has significant implications on cell death linked to cardiomyopathy, tumorigenesis, and cerebral hemorrhage to name a few. Here we summarize current literature on ferroptosis, including organelle dysfunction, signaling transduction pathways, metabolic reprogramming and epigenetic regulators in cancer progression. With regard to organelles, mitochondria-induced cysteine starvation, endoplasmic reticulum-related oxidative stress, lysosome dysfunction and golgi stress-related lipid peroxidation all contribute to induction of ferroptosis. Understanding the underlying mechanism in ferroptosis could provide insight into the treatment of various intractable diseases including cancers.

Published
2020
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2. The epigenetic regulators and metabolic changes in ferroptosis-associated cancer progression.

Author

Wu, Yuqing, Zhang, Siwei, Gong, Xiaoxiao, Tam, Samantha, Xiao, Desheng, Liu, Shuang, and Tao, Yongguang

Subjects
CANCER invasiveness, CELL morphology, GENETICS, CELL death, CEREBRAL hemorrhage
Abstract

Ferroptosis, a novel form of regulated cell death, is different from other types of cell death in morphology, genetics and biochemistry. Increasing evidence indicates that ferroptosis has significant implications on cell death linked to cardiomyopathy, tumorigenesis, and cerebral hemorrhage to name a few. Here we summarize current literature on ferroptosis, including organelle dysfunction, signaling transduction pathways, metabolic reprogramming and epigenetic regulators in cancer progression. With regard to organelles, mitochondria-induced cysteine starvation, endoplasmic reticulum-related oxidative stress, lysosome dysfunction and golgi stress-related lipid peroxidation all contribute to induction of ferroptosis. Understanding the underlying mechanism in ferroptosis could provide insight into the treatment of various intractable diseases including cancers. [ABSTRACT FROM AUTHOR]

Published
2020
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3. Brg-1 mediates the constitutive and fenretinide-induced expression of SPARC in mammary carcinoma cells via its interaction with transcription factor Sp1

Author

Yong Zhong Xu, M. Heravi, Danuta Radzioch, Thusanth Thuraisingam, Thierry Muanza, and Sergio Di Marco

Subjects
Cancer Research, Fenretinide, Sp1 Transcription Factor, Molecular Sequence Data, Chromatin Remodeling Factor, Biology, lcsh:RC254-282, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Tumor Cells, Cultured, Transcriptional regulation, Animals, Osteonectin, Promoter Regions, Genetic, Transcription factor, 030304 developmental biology, 0303 health sciences, Sp1 transcription factor, Base Sequence, Research, Matricellular protein, DNA Helicases, Mammary Neoplasms, Experimental, Nuclear Proteins, Promoter, DNA, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, 3. Good health, Gene Expression Regulation, Neoplastic, chemistry, Oncology, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Molecular Medicine, Transcription Factors
Abstract

Background Secreted protein, acidic and rich in cysteine (SPARC) is a matricellular protein that mediates cell-matrix interactions. It has been shown, depending on the type of cancer, to possess either pro- or anti-tumorigenic properties. The transcriptional regulation of the SPARC gene expression has not been fully elucidated and the effects of anti-cancer drugs on this process have not been explored. Results In the present study, we demonstrated that chromatin remodeling factor Brg-1 is recruited to the proximal SPARC promoter region (-130/-56) through an interaction with transcription factor Sp1. We identified Brg-1 as a critical regulator for the constitutive expression levels of SPARC mRNA and protein in mammary carcinoma cell lines and for SPARC secretion into culture media. Furthermore, we found that Brg-1 cooperates with Sp1 to enhance SPARC promoter activity. Interestingly, fenretinide [N-4(hydroxyphenyl) retinamide, 4-HPR], a synthetic retinoid with anti-cancer properties, was found to up-regulate the transcription, expression and secretion of SPARC via induction of the Brg-1 in a dose-dependent manner. Finally, our results demonstrated that fenretinide-induced expression of SPARC contributes significantly to a decreased invasion of mammary carcinoma cells. Conclusions Overall, our results reveal a novel cooperative role of Brg-1 and Sp1 in mediating the constitutive and fenretinide-induced expression of SPARC, and provide new insights for the understanding of the anti-cancer effects of fenretinide.

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