JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation
Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Qi, Jia [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Rechteinformationen: |
Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine |
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| Übergeordnetes Werk: |
Enthalten in: The American journal of Chinese medicine - Garden City, NY : Inst., 1973, 43(2015), 2, Seite 337-347 |
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| Übergeordnetes Werk: |
volume:43 ; year:2015 ; number:2 ; pages:337-347 |
| Links: |
|---|
| DOI / URN: |
10.1142/S0192415X15500226 |
|---|
| Katalog-ID: |
OLC1965339697 |
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| 520 | |a Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. | ||
| 540 | |a Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine | ||
| 650 | 4 | |a Breast Neoplasms - genetics | |
| 650 | 4 | |a Triterpenes - therapeutic use | |
| 650 | 4 | |a Transcription, Genetic - drug effects | |
| 650 | 4 | |a Triterpenes - pharmacology | |
| 650 | 4 | |a Cell Transformation, Neoplastic - drug effects | |
| 650 | 4 | |a Tumor Microenvironment - genetics | |
| 650 | 4 | |a Tumor Microenvironment - drug effects | |
| 650 | 4 | |a Vascular Endothelial Growth Factor A - genetics | |
| 650 | 4 | |a Cell Survival - drug effects | |
| 650 | 4 | |a STAT3 Transcription Factor - metabolism | |
| 650 | 4 | |a STAT3 Transcription Factor - physiology | |
| 650 | 4 | |a Phosphorylation - drug effects | |
| 650 | 4 | |a Signal Transduction - drug effects | |
| 650 | 4 | |a Cell Movement - drug effects | |
| 650 | 4 | |a Breast Neoplasms - pathology | |
| 650 | 4 | |a Breast Neoplasms - blood supply | |
| 650 | 4 | |a Neovascularization, Pathologic - drug therapy | |
| 650 | 4 | |a Cell Adhesion - drug effects | |
| 650 | 4 | |a Autocrine Communication - drug effects | |
| 700 | 1 | |a Xia, Ge |4 oth | |
| 700 | 1 | |a Huang, Cheng Rong |4 oth | |
| 700 | 1 | |a Wang, Jian Xia |4 oth | |
| 700 | 1 | |a Zhang, Jian |4 oth | |
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10.1142/S0192415X15500226 doi PQ20160617 (DE-627)OLC1965339697 (DE-599)GBVOLC1965339697 (PRQ)p1246-da4fc540fc9d2f20a22ec06aa4037e2f5a6080d14a7b1556f8bc87ac342720470 (KEY)0043278420150000043000200337jsi124cucurbitaciniinhibitstumorangiogenesisofhuma DE-627 ger DE-627 rakwb eng 610 DNB 44.00 bkl Qi, Jia verfasserin aut JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine Breast Neoplasms - genetics Triterpenes - therapeutic use Transcription, Genetic - drug effects Triterpenes - pharmacology Cell Transformation, Neoplastic - drug effects Tumor Microenvironment - genetics Tumor Microenvironment - drug effects Vascular Endothelial Growth Factor A - genetics Cell Survival - drug effects STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - physiology Phosphorylation - drug effects Signal Transduction - drug effects Cell Movement - drug effects Breast Neoplasms - pathology Breast Neoplasms - blood supply Neovascularization, Pathologic - drug therapy Cell Adhesion - drug effects Autocrine Communication - drug effects Xia, Ge oth Huang, Cheng Rong oth Wang, Jian Xia oth Zhang, Jian oth Enthalten in The American journal of Chinese medicine Garden City, NY : Inst., 1973 43(2015), 2, Seite 337-347 (DE-627)166447161 (DE-600)193085-0 (DE-576)038676486 0090-2942 nnns volume:43 year:2015 number:2 pages:337-347 http://dx.doi.org/10.1142/S0192415X15500226 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25787299 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-OAS SSG-OLC-MFO GBV_ILN_4012 44.00 AVZ AR 43 2015 2 337-347 |
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10.1142/S0192415X15500226 doi PQ20160617 (DE-627)OLC1965339697 (DE-599)GBVOLC1965339697 (PRQ)p1246-da4fc540fc9d2f20a22ec06aa4037e2f5a6080d14a7b1556f8bc87ac342720470 (KEY)0043278420150000043000200337jsi124cucurbitaciniinhibitstumorangiogenesisofhuma DE-627 ger DE-627 rakwb eng 610 DNB 44.00 bkl Qi, Jia verfasserin aut JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine Breast Neoplasms - genetics Triterpenes - therapeutic use Transcription, Genetic - drug effects Triterpenes - pharmacology Cell Transformation, Neoplastic - drug effects Tumor Microenvironment - genetics Tumor Microenvironment - drug effects Vascular Endothelial Growth Factor A - genetics Cell Survival - drug effects STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - physiology Phosphorylation - drug effects Signal Transduction - drug effects Cell Movement - drug effects Breast Neoplasms - pathology Breast Neoplasms - blood supply Neovascularization, Pathologic - drug therapy Cell Adhesion - drug effects Autocrine Communication - drug effects Xia, Ge oth Huang, Cheng Rong oth Wang, Jian Xia oth Zhang, Jian oth Enthalten in The American journal of Chinese medicine Garden City, NY : Inst., 1973 43(2015), 2, Seite 337-347 (DE-627)166447161 (DE-600)193085-0 (DE-576)038676486 0090-2942 nnns volume:43 year:2015 number:2 pages:337-347 http://dx.doi.org/10.1142/S0192415X15500226 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25787299 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-OAS SSG-OLC-MFO GBV_ILN_4012 44.00 AVZ AR 43 2015 2 337-347 |
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10.1142/S0192415X15500226 doi PQ20160617 (DE-627)OLC1965339697 (DE-599)GBVOLC1965339697 (PRQ)p1246-da4fc540fc9d2f20a22ec06aa4037e2f5a6080d14a7b1556f8bc87ac342720470 (KEY)0043278420150000043000200337jsi124cucurbitaciniinhibitstumorangiogenesisofhuma DE-627 ger DE-627 rakwb eng 610 DNB 44.00 bkl Qi, Jia verfasserin aut JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine Breast Neoplasms - genetics Triterpenes - therapeutic use Transcription, Genetic - drug effects Triterpenes - pharmacology Cell Transformation, Neoplastic - drug effects Tumor Microenvironment - genetics Tumor Microenvironment - drug effects Vascular Endothelial Growth Factor A - genetics Cell Survival - drug effects STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - physiology Phosphorylation - drug effects Signal Transduction - drug effects Cell Movement - drug effects Breast Neoplasms - pathology Breast Neoplasms - blood supply Neovascularization, Pathologic - drug therapy Cell Adhesion - drug effects Autocrine Communication - drug effects Xia, Ge oth Huang, Cheng Rong oth Wang, Jian Xia oth Zhang, Jian oth Enthalten in The American journal of Chinese medicine Garden City, NY : Inst., 1973 43(2015), 2, Seite 337-347 (DE-627)166447161 (DE-600)193085-0 (DE-576)038676486 0090-2942 nnns volume:43 year:2015 number:2 pages:337-347 http://dx.doi.org/10.1142/S0192415X15500226 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25787299 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-OAS SSG-OLC-MFO GBV_ILN_4012 44.00 AVZ AR 43 2015 2 337-347 |
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10.1142/S0192415X15500226 doi PQ20160617 (DE-627)OLC1965339697 (DE-599)GBVOLC1965339697 (PRQ)p1246-da4fc540fc9d2f20a22ec06aa4037e2f5a6080d14a7b1556f8bc87ac342720470 (KEY)0043278420150000043000200337jsi124cucurbitaciniinhibitstumorangiogenesisofhuma DE-627 ger DE-627 rakwb eng 610 DNB 44.00 bkl Qi, Jia verfasserin aut JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. Nutzungsrecht: © 2015, World Scientific Publishing Company & Institute for Advanced Research in Asian Science and Medicine Breast Neoplasms - genetics Triterpenes - therapeutic use Transcription, Genetic - drug effects Triterpenes - pharmacology Cell Transformation, Neoplastic - drug effects Tumor Microenvironment - genetics Tumor Microenvironment - drug effects Vascular Endothelial Growth Factor A - genetics Cell Survival - drug effects STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - physiology Phosphorylation - drug effects Signal Transduction - drug effects Cell Movement - drug effects Breast Neoplasms - pathology Breast Neoplasms - blood supply Neovascularization, Pathologic - drug therapy Cell Adhesion - drug effects Autocrine Communication - drug effects Xia, Ge oth Huang, Cheng Rong oth Wang, Jian Xia oth Zhang, Jian oth Enthalten in The American journal of Chinese medicine Garden City, NY : Inst., 1973 43(2015), 2, Seite 337-347 (DE-627)166447161 (DE-600)193085-0 (DE-576)038676486 0090-2942 nnns volume:43 year:2015 number:2 pages:337-347 http://dx.doi.org/10.1142/S0192415X15500226 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25787299 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-OAS SSG-OLC-MFO GBV_ILN_4012 44.00 AVZ AR 43 2015 2 337-347 |
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610 DNB 44.00 bkl JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation Breast Neoplasms - genetics Triterpenes - therapeutic use Transcription, Genetic - drug effects Triterpenes - pharmacology Cell Transformation, Neoplastic - drug effects Tumor Microenvironment - genetics Tumor Microenvironment - drug effects Vascular Endothelial Growth Factor A - genetics Cell Survival - drug effects STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - physiology Phosphorylation - drug effects Signal Transduction - drug effects Cell Movement - drug effects Breast Neoplasms - pathology Breast Neoplasms - blood supply Neovascularization, Pathologic - drug therapy Cell Adhesion - drug effects Autocrine Communication - drug effects |
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jsi-124 (cucurbitacin i) inhibits tumor angiogenesis of human breast cancer through reduction of stat3 phosphorylation |
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JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation |
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Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. |
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Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. |
| abstract_unstemmed |
Breast cancer (BC) is the most frequently diagnosed type of cancer all over the world. Angiogenesis, a physiological or pathological process characterized by the sprouting of new blood vessels from existing vessels, plays a vital role in tumor nutrition. In this work, we used JSI-124 (Cucurbitacin I), a selective JAK/STAT3 signaling pathway inhibitor, to investigate the role of STAT3 in tumor angiogenesis of a human BC cell line in vitro. JSI-124 inhibited cell viability, proliferation, adhesion, migration and tube formation of a human BC cell line MDA-MB-468. After transfection with pMXs-Stat3C, a dominant active mutant, the inhibitory effects of JSI-124 on MDA-MB-468 were abolished. Furthermore, JSI-124 reduced the phosphorylation of STAT3. These results suggested that JSI-124 inhibited tumor angiogenesis of the human BC cell line in vitro through the reduction of STAT3 phosphorylation. In addition, JSI-124 could reduce VEGF transcription and secretion, suggesting that JSI-124 is also involved in the inhibition of the VEGF autocrine loop in the tumor microenvironment. |
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JSI-124 (Cucurbitacin I) Inhibits Tumor Angiogenesis of Human Breast Cancer Through Reduction of STAT3 Phosphorylation |
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