LIVIVO - Search results -

Search results

Result 1 - 10 of total 10

Search options

Article ; Online: VEGFA activates an epigenetic pathway upregulating ovarian cancer-initiating cells.

Jang, Kibeom / Kim, Minsoon / Gilbert, Candace A / Simpkins, Fiona / Ince, Tan A / Slingerland, Joyce M

2017 Volume 9, Issue 3, Page(s) 304–318

Abstract: The angiogenic factor, VEGFA, is a therapeutic target in ovarian cancer (OVCA). VEGFA can also stimulate stem-like cells in certain cancers, but mechanisms thereof are poorly understood. Here, we show that VEGFA mediates stem cell actions in primary ... ...

Abstract	The angiogenic factor, VEGFA, is a therapeutic target in ovarian cancer (OVCA). VEGFA can also stimulate stem-like cells in certain cancers, but mechanisms thereof are poorly understood. Here, we show that VEGFA mediates stem cell actions in primary human OVCA culture and OVCA lines via VEGFR2-dependent Src activation to upregulate Bmi1, tumor spheres, and ALDH1 activity. The VEGFA-mediated increase in spheres was abrogated by Src inhibition or
MeSH term(s)	Aldehyde Dehydrogenase 1 Family ; Cell Line, Tumor ; Cell Proliferation ; Epigenesis, Genetic ; Female ; Humans ; Isoenzymes/metabolism ; MicroRNAs/metabolism ; Neoplastic Stem Cells/physiology ; Ovarian Neoplasms/pathology ; Polycomb Repressive Complex 1/metabolism ; Retinal Dehydrogenase/metabolism ; Up-Regulation ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	BMI1 protein, human ; Isoenzymes ; MIRN128 microRNA, human ; MicroRNAs ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Aldehyde Dehydrogenase 1 Family (EC 1.2.1) ; ALDH1A1 protein, human (EC 1.2.1.36) ; Retinal Dehydrogenase (EC 1.2.1.36) ; Polycomb Repressive Complex 1 (EC 2.3.2.27)
Language	English
Publishing date	2017-02-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.201606840
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6784: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: p27 transcriptionally coregulates cJun to drive programs of tumor progression.

Yoon, Hyunho / Kim, Minsoon / Jang, Kibeom / Shin, Miyoung / Besser, Alexandra / Xiao, Xue / Zhao, Dekuang / Wander, Seth A / Briegel, Karoline / Morey, Lluis / Minn, Andy / Slingerland, Joyce M

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 14, Page(s) 7005–7014

Abstract: p27 shifts from CDK inhibitor to oncogene when phosphorylated by PI3K effector kinases. Here, we show that p27 is a cJun coregulator, whose assembly and chromatin association is governed by p27 phosphorylation. In breast and bladder cancer cells with ... ...

Abstract	p27 shifts from CDK inhibitor to oncogene when phosphorylated by PI3K effector kinases. Here, we show that p27 is a cJun coregulator, whose assembly and chromatin association is governed by p27 phosphorylation. In breast and bladder cancer cells with high p27pT157pT198 or expressing a CDK-binding defective p27pT157pT198 phosphomimetic (p27CK-DD), cJun is activated and interacts with p27, and p27/cJun complexes localize to the nucleus. p27/cJun up-regulates
MeSH term(s)	Cell Adhesion ; Cell Line, Tumor ; Cell Movement ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	CDKN1B protein, human ; Proto-Oncogene Proteins c-jun ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2019-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1817415116
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: MYC

Dhanasekaran, Renumathy / Baylot, Virginie / Kim, Minsoon / Kuruvilla, Sibu / Bellovin, David I / Adeniji, Nia / Rajan Kd, Anand / Lai, Ian / Gabay, Meital / Tong, Ling / Krishnan, Maya / Park, Jangho / Hu, Theodore / Barbhuiya, Mustafa A / Gentles, Andrew J / Kannan, Kasthuri / Tran, Phuoc T / Felsher, Dean W

eLife

2020 Volume 9

Abstract: Metastasis is a major cause of cancer mortality. We generated an autochthonous transgenic mouse model whereby conditional expression ... ...

Abstract	Metastasis is a major cause of cancer mortality. We generated an autochthonous transgenic mouse model whereby conditional expression of
MeSH term(s)	Animals ; Cell Line, Tumor ; Chemokine CCL2/metabolism ; Epithelial-Mesenchymal Transition ; Fibrosis/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity, Innate ; Interleukin-13/metabolism ; Macrophages/immunology ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasms/metabolism ; Nuclear Proteins/metabolism ; Principal Component Analysis ; Proto-Oncogene Proteins c-myc/metabolism ; RAW 264.7 Cells ; Sequence Analysis, RNA ; Signal Transduction ; Tumor Microenvironment/physiology ; Twist-Related Protein 1/metabolism
Chemical Substances	CCL2 protein, human ; Ccl2 protein, mouse ; Chemokine CCL2 ; Interleukin-13 ; MYC protein, human ; Myc protein, mouse ; Nuclear Proteins ; Proto-Oncogene Proteins c-myc ; TWIST1 protein, human ; Twist-Related Protein 1 ; Twist1 protein, mouse (136253-27-5)
Language	English
Publishing date	2020-01-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.50731
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Down-regulation of Notch-dependent transcription by Akt in vitro.

Song, Jieun / Park, Sungwoo / Kim, Minsoon / Shin, Incheol

FEBS letters

2008 Volume 582, Issue 12, Page(s) 1693–1699

Abstract: The effect of Akt on Notch intracellular domain (NICD)-mediated transcription was investigated. Transfection experiments revealed that constitutively active Akt down-regulates NICD-dependent transcription. Kinase inactive dominant negative Akt did not ... ...

Abstract	The effect of Akt on Notch intracellular domain (NICD)-mediated transcription was investigated. Transfection experiments revealed that constitutively active Akt down-regulates NICD-dependent transcription. Kinase inactive dominant negative Akt did not affect NICD transcriptional activity, indicating that Akt kinase activity is responsible for the down-regulation. Studies using histone deacetylase (HDAC) and silencing mediator of retinoid and thyroid hormone receptor (SMRT) revealed that modulation of NICD transcriptional activity is not mediated by an HDAC-dependent mechanism or recruitment of the co-repressor SMRT. Akt inhibited proper nuclear localization of NICD, and phosphorylated NICD both in vitro and caused its hyperphosphorylation in vivo. These results may suggest possible regulation of NICD transcriptional activity by Akt-mediated phosphorylation and subsequent inhibition of proper nuclear localization of NICD.
MeSH term(s)	Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Nucleus/metabolism ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Histone Deacetylases/metabolism ; Humans ; Isoenzymes/metabolism ; Nuclear Receptor Co-Repressor 2 ; Phosphorylation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Notch/metabolism ; Repressor Proteins/metabolism ; Transcription, Genetic ; Transfection
Chemical Substances	DNA-Binding Proteins ; Isoenzymes ; NCOR2 protein, human ; Nuclear Receptor Co-Repressor 2 ; Receptors, Notch ; Repressor Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2008-05-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2008.04.024
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.B 282: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: PTEN sensitizes MDA-MB-468 cells to inhibition of MEK/Erk signaling for the blockade of cell proliferation.

Jang, Kibeom / Kim, Minsoon / Seo, Hye-Sook / Shin, Incheol

Oncology reports

2010 Volume 24, Issue 3, Page(s) 787–793

Abstract: Phosphatase and tensin homolog (PTEN) is a tumor suppressor that inhibits PI3K/Akt signaling. To examine the effect of PTEN on breast cancer cell proliferation, we expressed PTEN in MDA-MB-468 cells (MDA-MB-468 PTEN) by retroviral infection and tested ... ...

Abstract	Phosphatase and tensin homolog (PTEN) is a tumor suppressor that inhibits PI3K/Akt signaling. To examine the effect of PTEN on breast cancer cell proliferation, we expressed PTEN in MDA-MB-468 cells (MDA-MB-468 PTEN) by retroviral infection and tested the cell proliferation rate. We found that the growth rate of MDA-MB-468 PTEN cells was significantly lower than that of MDA-MB-468 control vector cells (MDA-MB-468 vec). When the PI3K/Akt signaling inhibitor LY294002 and the MEK/Erk signaling inhibitor U0126 were applied, LY294002 reduced cell proliferation in MDA-MB-468 PTEN and MDA-MB-468 vec by 20%, while U0126 led to a >60% reduction in MDA-MB-468 PTEN and a 20% reduction in MDA-MB-468 vec cells. FACS analysis demonstrated that the subG0/G1 apoptotic fraction was significantly increased in MDA-MB-468 PTEN cells after U0126 treatment, while LY294002 treatment in both cell lines and U0126 treatment in MDA-MB-468 vec cells led to a modest increase in the apoptotic fraction. This phenomenon was accompanied by the down-regulation of p-Erk. p-Erk levels were significantly lower after U0126 treatment in MDA-MB-468 PTEN cells. Similar results were observed in MDA-MB-231 cells, which express endogenous PTEN. The growth of MDA-MB-231 cells was significantly inhibited after U0126 treatment, compared to LY294002, while PTEN-null ZR-75-1 cells did not show increased sensitivity to U0126 over LY294002. Taken together, these findings suggest that blockade of PI3K/Akt signaling by PTEN may render breast cancer cells more dependent on the MEK/Erk pathway for their proliferation and survival.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Butadienes/pharmacology ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Chromones/pharmacology ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Humans ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/metabolism ; Morpholines/pharmacology ; Nitriles/pharmacology ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Time Factors ; Transfection
Chemical Substances	Antineoplastic Agents ; Butadienes ; Chromones ; Morpholines ; Nitriles ; Protein Kinase Inhibitors ; U 0126 ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Language	English
Publishing date	2010-07-27
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1222484-4
ISSN	1791-2431 ; 1021-335X
ISSN (online)	1791-2431
ISSN	1021-335X
DOI	10.3892/or_00000922
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4213: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Protein kinase Cδ negatively regulates Notch1-dependent transcription via a kinase-independent mechanism in vitro

Kim, Minsoon / Ju, Ji-hyun / Jang, Kibeom / Oh, Sunhwa / Song, Jieun / Kim, Chul Geun / Shin, Incheol

Biochimica et biophysica acta. Molecular cell research. 2012 Feb., v. 1823, no. 2

2012

Abstract: Protein kinase Cδ (PKCδ) plays a significant role in the regulation of growth, apoptosis, and differentiation in a diversity of cell types. We investigated the effect of PKCδ on Notch1 intracellular domain (NICD)-mediated transcription with Notch ... ...

Abstract	Protein kinase Cδ (PKCδ) plays a significant role in the regulation of growth, apoptosis, and differentiation in a diversity of cell types. We investigated the effect of PKCδ on Notch1 intracellular domain (NICD)-mediated transcription with Notch transcription reporter constructs. The results indicate that co-expression of PKCδ down-regulated NICD-dependent transcription. Co-expression of a dominant negative PKCδ (K376R) variant lacking kinase activity was also able to downregulate NICD-dependent transcription, suggesting that PKCδ exerts its inhibitory effect via a kinase-independent mechanism(s). Interestingly, expression of PKCδ as well as K376R induced NICD up-regulation by inhibiting proteasome-mediated degradation of NICD, indicating that NICD protein quantity is not proportional to its transcriptional activity. When the subcellular distribution of NICD was investigated by both subcellular fractionation and immunocytochemistry, it was found that PKCδ and K376R effectively impaired proper nuclear localization of NICD, possibly via a physical association between NICD and PKCδ, which was confirmed by co-immunoprecipitation experiments. Chromatin immunoprecipitation assays revealed that both PKCδ and K376R inhibit the association of NICD with the promoter region of its target gene, Hes1. Furthermore, silencing of PKCδ resulted in increased NICD nuclear localization and NICD transcriptional activity in MCF-7 cells. PKCδ silencing-induced increase in anti-apoptotic survivin could not rescue apoptosis induced by doxorubicin. The data herein indicate that PKCδ can induce down-regulation of NICD transcriptional activity via a kinase-independent inhibition of NICD nuclear targeting and dissociation of NICD from target gene promoters.
Keywords	apoptosis ; chromatin ; dissociation ; doxorubicin ; fractionation ; gene expression regulation ; genes ; immunocytochemistry ; precipitin tests ; promoter regions ; protein kinase C ; transcription (genetics)
Language	English
Dates of publication	2012-02
Size	p. 387-397.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	283444-3
ISSN	0167-4889
ISSN	0167-4889
DOI	10.1016/j.bbamcr.2011.11.005
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Dual Src and MEK Inhibition Decreases Ovarian Cancer Growth and Targets Tumor Initiating Stem-Like Cells.

Simpkins, Fiona / Jang, Kibeom / Yoon, Hyunho / Hew, Karina E / Kim, Minsoon / Azzam, Diana J / Sun, Jun / Zhao, Dekuang / Ince, Tan A / Liu, Wenbin / Guo, Wei / Wei, Zhi / Zhang, Gao / Mills, Gordon B / Slingerland, Joyce M

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 24, Issue 19, Page(s) 4874–4886

Abstract: Purpose: ...

Abstract	Purpose:
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Apoptosis/drug effects ; Benzimidazoles/pharmacology ; Benzodioxoles/administration & dosage ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease-Free Survival ; Drug Resistance, Neoplasm ; Estrogen Receptor alpha/genetics ; Female ; Humans ; MAP Kinase Kinase 1/antagonists & inhibitors ; MAP Kinase Kinase 1/genetics ; Mice ; Middle Aged ; Neoplastic Stem Cells/drug effects ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Protein Kinase Inhibitors/administration & dosage ; Proteomics ; Quinazolines/administration & dosage ; Xenograft Model Antitumor Assays ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/genetics
Chemical Substances	AZD 6244 ; Benzimidazoles ; Benzodioxoles ; Estrogen Receptor alpha ; Protein Kinase Inhibitors ; Quinazolines ; saracatinib (9KD24QGH76) ; src-Family Kinases (EC 2.7.10.2) ; MAP Kinase Kinase 1 (EC 2.7.12.2)
Language	English
Publishing date	2018-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-17-3697
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4223: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Protein kinase Cδ negatively regulates Notch1-dependent transcription via a kinase-independent mechanism in vitro.

Kim, Minsoon / Ju, Ji-hyun / Jang, Kibeom / Oh, Sunhwa / Song, Jieun / Kim, Chul Geun / Shin, Incheol

Biochimica et biophysica acta

2012 Volume 1823, Issue 2, Page(s) 387–397

Abstract	Protein kinase Cδ (PKCδ) plays a significant role in the regulation of growth, apoptosis, and differentiation in a diversity of cell types. We investigated the effect of PKCδ on Notch1 intracellular domain (NICD)-mediated transcription with Notch transcription reporter constructs. The results indicate that co-expression of PKCδ down-regulated NICD-dependent transcription. Co-expression of a dominant negative PKCδ (K376R) variant lacking kinase activity was also able to downregulate NICD-dependent transcription, suggesting that PKCδ exerts its inhibitory effect via a kinase-independent mechanism(s). Interestingly, expression of PKCδ as well as K376R induced NICD up-regulation by inhibiting proteasome-mediated degradation of NICD, indicating that NICD protein quantity is not proportional to its transcriptional activity. When the subcellular distribution of NICD was investigated by both subcellular fractionation and immunocytochemistry, it was found that PKCδ and K376R effectively impaired proper nuclear localization of NICD, possibly via a physical association between NICD and PKCδ, which was confirmed by co-immunoprecipitation experiments. Chromatin immunoprecipitation assays revealed that both PKCδ and K376R inhibit the association of NICD with the promoter region of its target gene, Hes1. Furthermore, silencing of PKCδ resulted in increased NICD nuclear localization and NICD transcriptional activity in MCF-7 cells. PKCδ silencing-induced increase in anti-apoptotic survivin could not rescue apoptosis induced by doxorubicin. The data herein indicate that PKCδ can induce down-regulation of NICD transcriptional activity via a kinase-independent inhibition of NICD nuclear targeting and dissociation of NICD from target gene promoters.
MeSH term(s)	Animals ; Cell Line ; Cell Proliferation ; Cell Survival ; Down-Regulation ; Gene Expression Regulation ; Gene Silencing ; Genes, Reporter ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Mice ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Protein Kinase C-delta/genetics ; Protein Kinase C-delta/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Transcription, Genetic
Chemical Substances	Notch1 protein, mouse ; Receptor, Notch1 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Protein Kinase C-delta (EC 2.7.11.13) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2012-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2011.11.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: CD24 enhances DNA damage-induced apoptosis by modulating NF-κB signaling in CD44-expressing breast cancer cells.

Ju, Ji-hyun / Jang, Kibeom / Lee, Kyung-Min / Kim, Minsoon / Kim, Jongbin / Yi, Jae Youn / Noh, Dong-Young / Shin, Incheol

Carcinogenesis

2011 Volume 32, Issue 10, Page(s) 1474–1483

Abstract: Cluster of differentiation 24 (CD24) is a small glycosylphosphatidylinositol-linked cell surface molecule that is expressed in a variety of human carcinomas, including breast cancer. To determine the role of CD24 in breast cancer cells, we expressed CD24 ...

Abstract	Cluster of differentiation 24 (CD24) is a small glycosylphosphatidylinositol-linked cell surface molecule that is expressed in a variety of human carcinomas, including breast cancer. To determine the role of CD24 in breast cancer cells, we expressed CD24 in CD24-negative/low and cluster of differentiation 44 (CD44)-positive MDA-MB-231 metastatic breast cancer cells. Forced expression of CD24 resulted in a decrease in c-Raf/mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein kinase signaling and reduced cell proliferation. Apoptosis induced by DNA damage was greatly enhanced in MDA-MB-231 CD24 cells as compared with MDA-MB-231 vec cells. CD24 expression efficiently attenuated DNA damage-induced nuclear factor-kappaB (NF-κB) signaling in MDA-MB-231 cells. However, in CD24-positive and CD44-negative/low MCF-7 cells, knockdown of CD24 did not significantly affect DNA damage-induced apoptosis nor NF-κB signaling. Silencing of CD24 in CD24/CD44-double-positive MDA-MB-468 cells partially rescued DNA damage-induced apoptosis. Transient transfection studies with 293T cells also revealed that CD24 attenuated cell viability and NF-κB signaling only when CD44 was cotransfected. These data indicate that CD24 expression potentiated DNA-induced apoptosis by suppressing antiapoptotic NF-κB signaling in CD44-expressing cells.
MeSH term(s)	Antibiotics, Antineoplastic/pharmacology ; Apoptosis ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; CD24 Antigen/chemistry ; CD24 Antigen/genetics ; CD24 Antigen/metabolism ; Cell Cycle/drug effects ; Cell Cycle/radiation effects ; Cell Differentiation/drug effects ; Cell Differentiation/radiation effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/radiation effects ; DNA Damage ; Doxorubicin/pharmacology ; Extracellular Signal-Regulated MAP Kinases/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Flow Cytometry ; Humans ; Luciferases/metabolism ; Mitogen-Activated Protein Kinases/genetics ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Neoplasm Invasiveness ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Radiation, Ionizing ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tumor Cells, Cultured
Chemical Substances	Antibiotics, Antineoplastic ; CD24 Antigen ; NF-kappa B ; RNA, Messenger ; RNA, Small Interfering ; Doxorubicin (80168379AG) ; Luciferases (EC 1.13.12.-) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2011-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgr173
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1558: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Interactions between Adipocytes and Breast Cancer Cells Stimulate Cytokine Production and Drive Src/Sox2/miR-302b-Mediated Malignant Progression.

Cancer research

2016 Volume 76, Issue 2, Page(s) 491–504

Abstract: Consequences of the obesity epidemic on cancer morbidity and mortality are not fully appreciated. Obesity is a risk factor for many cancers, but the mechanisms by which it contributes to cancer development and patient outcome have yet to be fully ... ...

Abstract	Consequences of the obesity epidemic on cancer morbidity and mortality are not fully appreciated. Obesity is a risk factor for many cancers, but the mechanisms by which it contributes to cancer development and patient outcome have yet to be fully elucidated. Here, we examined the effects of coculturing human-derived adipocytes with established and primary breast cancer cells on tumorigenic potential. We found that the interaction between adipocytes and cancer cells increased the secretion of proinflammatory cytokines. Prolonged culture of cancer cells with adipocytes or cytokines increased the proportion of mammosphere-forming cells and of cells expressing stem-like markers in vitro. Furthermore, contact with immature adipocytes increased the abundance of cancer cells with tumor-forming and metastatic potential in vivo. Mechanistic investigations demonstrated that cancer cells cultured with immature adipocytes or cytokines activated Src, thus promoting Sox2, c-Myc, and Nanog upregulation. Moreover, Sox2-dependent induction of miR-302b further stimulated cMYC and SOX2 expression and potentiated the cytokine-induced cancer stem cell-like properties. Finally, we found that Src inhibitors decreased cytokine production after coculture, indicating that Src is not only activated by adipocyte or cytokine exposures, but is also required to sustain cytokine induction. These data support a model in which cancer cell invasion into local fat would establish feed-forward loops to activate Src, maintain proinflammatory cytokine production, and increase tumor-initiating cell abundance and metastatic progression. Collectively, our findings reveal new insights underlying increased breast cancer mortality in obese individuals and provide a novel preclinical rationale to test the efficacy of Src inhibitors for breast cancer treatment.
MeSH term(s)	Adipocytes/cytology ; Adipocytes/metabolism ; Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cytokines/metabolism ; Disease Progression ; Female ; Humans ; Mice ; Obesity/complications ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; SOXB1 Transcription Factors ; Signal Transduction ; Transfection ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
Chemical Substances	Cytokines ; RNA, Messenger ; SOX2 protein, human ; SOXB1 Transcription Factors ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2016-01-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-15-0927
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.135/5: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito