Molecular mechanisms of the anticancer action of fustin isolated from Cotinus coggygria Scop. in MDA-MB-231 triple-negative breast cancer cell line
The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysi...
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Published in | Zeitschrift für Naturforschung C. A journal of biosciences |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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30.09.2024
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Abstract | The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of
Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysis to evaluate apoptosis, necrosis, and mitochondrial integrity, wound healing assay to study fustin antimigratory potential and quantitative reverse transcription-polymerase chain reaction to analyze the expression of genes associated with cell cycle control, programmed cell death, metastasis, and epigenetic alterations. A complex network-based bioinformatic analysis was also employed for protein-protein network construction, hub genes identification, and functional enrichment. The results revealed a significant induction of early and late apoptotic and necrotic events, a slight alteration of the mitochondria-related fluorescence, and marked antimotility effect after fustin treatment. Of 34 analyzed genes, seven fustin targets were identified, of which
,
, and
were significantly enriched in pathways such as cell cycle, intrinsic apoptotic signaling pathway in response to DNA damage and generic transcription pathway. Our findings outline some molecular mechanisms of the anticancer action of fustin pointing it out as a potential oncotherapeutic agent and provide directions for future
research. |
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AbstractList | Abstract The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of Cotinus coggygria Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysis to evaluate apoptosis, necrosis, and mitochondrial integrity, wound healing assay to study fustin antimigratory potential and quantitative reverse transcription-polymerase chain reaction to analyze the expression of genes associated with cell cycle control, programmed cell death, metastasis, and epigenetic alterations. A complex network-based bioinformatic analysis was also employed for protein–protein network construction, hub genes identification, and functional enrichment. The results revealed a significant induction of early and late apoptotic and necrotic events, a slight alteration of the mitochondria-related fluorescence, and marked antimotility effect after fustin treatment. Of 34 analyzed genes, seven fustin targets were identified, of which CDKN1A , ATM , and MYC were significantly enriched in pathways such as cell cycle, intrinsic apoptotic signaling pathway in response to DNA damage and generic transcription pathway. Our findings outline some molecular mechanisms of the anticancer action of fustin pointing it out as a potential oncotherapeutic agent and provide directions for future in vivo research. The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysis to evaluate apoptosis, necrosis, and mitochondrial integrity, wound healing assay to study fustin antimigratory potential and quantitative reverse transcription-polymerase chain reaction to analyze the expression of genes associated with cell cycle control, programmed cell death, metastasis, and epigenetic alterations. A complex network-based bioinformatic analysis was also employed for protein-protein network construction, hub genes identification, and functional enrichment. The results revealed a significant induction of early and late apoptotic and necrotic events, a slight alteration of the mitochondria-related fluorescence, and marked antimotility effect after fustin treatment. Of 34 analyzed genes, seven fustin targets were identified, of which , , and were significantly enriched in pathways such as cell cycle, intrinsic apoptotic signaling pathway in response to DNA damage and generic transcription pathway. Our findings outline some molecular mechanisms of the anticancer action of fustin pointing it out as a potential oncotherapeutic agent and provide directions for future research. The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of Cotinus coggygria Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysis to evaluate apoptosis, necrosis, and mitochondrial integrity, wound healing assay to study fustin antimigratory potential and quantitative reverse transcription-polymerase chain reaction to analyze the expression of genes associated with cell cycle control, programmed cell death, metastasis, and epigenetic alterations. A complex network-based bioinformatic analysis was also employed for protein-protein network construction, hub genes identification, and functional enrichment. The results revealed a significant induction of early and late apoptotic and necrotic events, a slight alteration of the mitochondria-related fluorescence, and marked antimotility effect after fustin treatment. Of 34 analyzed genes, seven fustin targets were identified, of which CDKN1A, ATM, and MYC were significantly enriched in pathways such as cell cycle, intrinsic apoptotic signaling pathway in response to DNA damage and generic transcription pathway. Our findings outline some molecular mechanisms of the anticancer action of fustin pointing it out as a potential oncotherapeutic agent and provide directions for future in vivo research.The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from the heartwood of Cotinus coggygria Scop. in the triple-negative breast cancer cell line MDA-MB-231. For this purpose, we applied fluorescence microscopy analysis to evaluate apoptosis, necrosis, and mitochondrial integrity, wound healing assay to study fustin antimigratory potential and quantitative reverse transcription-polymerase chain reaction to analyze the expression of genes associated with cell cycle control, programmed cell death, metastasis, and epigenetic alterations. A complex network-based bioinformatic analysis was also employed for protein-protein network construction, hub genes identification, and functional enrichment. The results revealed a significant induction of early and late apoptotic and necrotic events, a slight alteration of the mitochondria-related fluorescence, and marked antimotility effect after fustin treatment. Of 34 analyzed genes, seven fustin targets were identified, of which CDKN1A, ATM, and MYC were significantly enriched in pathways such as cell cycle, intrinsic apoptotic signaling pathway in response to DNA damage and generic transcription pathway. Our findings outline some molecular mechanisms of the anticancer action of fustin pointing it out as a potential oncotherapeutic agent and provide directions for future in vivo research. |
Author | Gospodinova, Zlatina I Tesevic, Vele Novakovic, Miroslav Antov, Georgi G Krasteva, Natalia A Pavlov, Danail V Valcheva-Kuzmanova, Stefka V |
Author_xml | – sequence: 1 givenname: Georgi G surname: Antov fullname: Antov, Georgi G organization: Laboratory of Genome Dynamics and Stability, Institute of Plant Physiology and Genetics, Bulgarian Academy of Sciences, Sofia, Bulgaria – sequence: 2 givenname: Zlatina I surname: Gospodinova fullname: Gospodinova, Zlatina I organization: Laboratory of Genome Dynamics and Stability, Institute of Plant Physiology and Genetics, Bulgarian Academy of Sciences, Sofia, Bulgaria – sequence: 3 givenname: Miroslav surname: Novakovic fullname: Novakovic, Miroslav organization: Department of Chemistry, University of Belgrade - Institute of Chemistry, Technology and Metallurgy, National Institute of the Republic of Serbia, Belgrade, Serbia – sequence: 4 givenname: Vele surname: Tesevic fullname: Tesevic, Vele organization: University of Belgrade - Faculty of Chemistry, Belgrade, Serbia – sequence: 5 givenname: Natalia A surname: Krasteva fullname: Krasteva, Natalia A organization: Department of Electroinduced and Adhesive Properties, Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Sofia, Bulgaria – sequence: 6 givenname: Danail V surname: Pavlov fullname: Pavlov, Danail V organization: Department of Biochemistry, Molecular Medicine and Nutrigenomics with Laboratory of Nutrigenomics, Functional Foods and Nutraceuticals, Faculty of Pharmacy, Medical University "Prof. Dr. Paraskev Stoyanov", Varna, Bulgaria – sequence: 7 givenname: Stefka V surname: Valcheva-Kuzmanova fullname: Valcheva-Kuzmanova, Stefka V organization: Department of Pharmacology and Clinical Pharmacology and Therapeutics, Faculty of Medicine, Medical University "Prof. Dr. Paraskev Stoyanov", Varna, Bulgaria |
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Keywords | antimigratory potential fustin differentially expressed genes proapoptotic effects MDA-MB-231 |
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Snippet | The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin isolated from... Abstract The aim of the present work was to investigate some of the molecular mechanisms and targets of the anticancer action of the bioflavonoid fustin... |
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Title | Molecular mechanisms of the anticancer action of fustin isolated from Cotinus coggygria Scop. in MDA-MB-231 triple-negative breast cancer cell line |
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