2018
Remšík, Ján; Binó, Lucia; Kahounová, Zuzana; Kharaishvili, Gvantsa; Šimecková, Šárka; Fedr, Radek; Kucírková, Tereza; Lenárt, Sára; Muresan, Ximena Maria; Slabáková, Eva; Knopfová, Lucia; Bouchal, Jan; Král, Milan; Beneš, Petr; Soucek, Karel
Trop-2 plasticity is controlled by epithelial-to-mesenchymal transition. Journal Article
In: Carcinogenesis, vol. 39, no. 11, pp. 1411–1418, 2018, ISSN: 1460-2180 0143-3334, (Place: England).
Abstract | Links | BibTeX | Tags: Animals, Antigens, Breast Neoplasms/mortality/*pathology, Cadherins/biosynthesis, Carcinoma/*pathology, CD/biosynthesis, Cell Adhesion Molecules/genetics/*metabolism, Cell Line, Disease Progression, DNA Methylation/genetics, Epithelial Cells/*metabolism, Epithelial-Mesenchymal Transition/physiology, Female, Humans, Inbred BALB C, Male, Mice, Neoplasm/genetics/*metabolism, Prostatic Neoplasms/mortality/*pathology, Tumor, Xenograft Model Antitumor Assays
@article{remsik_trop-2_2018,
title = {Trop-2 plasticity is controlled by epithelial-to-mesenchymal transition.},
author = {Ján Remšík and Lucia Binó and Zuzana Kahounová and Gvantsa Kharaishvili and Šárka Šimecková and Radek Fedr and Tereza Kucírková and Sára Lenárt and Ximena Maria Muresan and Eva Slabáková and Lucia Knopfová and Jan Bouchal and Milan Král and Petr Beneš and Karel Soucek},
doi = {10.1093/carcin/bgy095},
issn = {1460-2180 0143-3334},
year = {2018},
date = {2018-12-01},
journal = {Carcinogenesis},
volume = {39},
number = {11},
pages = {1411–1418},
abstract = {The cell surface glycoprotein Trop-2 is commonly overexpressed in carcinomas and represents an exceptional antigen for targeted therapy. Here, we provide evidence that surface Trop-2 expression is functionally connected with an epithelial phenotype in breast and prostate cell lines and in patient tumor samples. We further show that Trop-2 expression is suppressed epigenetically or through the action of epithelial-to-mesenchymal transition transcription factors and that deregulation of Trop-2 expression is linked with cancer progression and poor patient prognosis. Moreover, our data suggest that the cancer plasticity-driven intratumoral heterogeneity in Trop-2 expression may significantly contribute to response and resistance to therapies targeting Trop-2-expressing cells.},
note = {Place: England},
keywords = {Animals, Antigens, Breast Neoplasms/mortality/*pathology, Cadherins/biosynthesis, Carcinoma/*pathology, CD/biosynthesis, Cell Adhesion Molecules/genetics/*metabolism, Cell Line, Disease Progression, DNA Methylation/genetics, Epithelial Cells/*metabolism, Epithelial-Mesenchymal Transition/physiology, Female, Humans, Inbred BALB C, Male, Mice, Neoplasm/genetics/*metabolism, Prostatic Neoplasms/mortality/*pathology, Tumor, Xenograft Model Antitumor Assays},
pubstate = {published},
tppubtype = {article}
}
2010
Starsíchová, Andrea; Lincová, Eva; Pernicová, Zuzana; Kozubík, Alois; Soucek, Karel
TGF-beta1 suppresses IL-6-induced STAT3 activation through regulation of Jak2 expression in prostate epithelial cells. Journal Article
In: Cellular signalling, vol. 22, no. 11, pp. 1734–1744, 2010, ISSN: 1873-3913 0898-6568, (Place: England).
Abstract | Links | BibTeX | Tags: Cell Line, Cell Proliferation, Epithelial Cells/*metabolism, Humans, Interleukin-6/*antagonists & inhibitors/pharmacology, Janus Kinase 2/genetics/*metabolism, Male, Mucin-1/metabolism, Phosphorylation, Prostate/cytology/enzymology/*metabolism, Prostatic Hyperplasia/enzymology/*metabolism, RNA, RNA Interference, Signal Transduction, Smad Proteins/metabolism, Small Interfering/metabolism, STAT3 Transcription Factor/*metabolism, Transforming Growth Factor beta1/*pharmacology
@article{starsichova_tgf-beta1_2010,
title = {TGF-beta1 suppresses IL-6-induced STAT3 activation through regulation of Jak2 expression in prostate epithelial cells.},
author = {Andrea Starsíchová and Eva Lincová and Zuzana Pernicová and Alois Kozubík and Karel Soucek},
doi = {10.1016/j.cellsig.2010.06.014},
issn = {1873-3913 0898-6568},
year = {2010},
date = {2010-11-01},
journal = {Cellular signalling},
volume = {22},
number = {11},
pages = {1734–1744},
abstract = {Chronic inflammation plays an important role in the initiation and progression of various human diseases including benign prostatic hyperplasia or prostate cancer. Here we show that the proinflammatory cytokine interleukin-6 (IL-6) has prosurvival effects and chronically activates the Jak2/STAT3 signalling pathway in a model of benign prostatic hyperplasia (BPH-1). We demonstrate that the antiinflammatory cytokine transforming growth factor-beta1 (TGF-beta1), which also permanently activates its canonical signalling pathway through SMAD proteins in BPH-1 cells, modifies the effects of IL-6 on cell proliferation. Importantly, TGF-beta1 inhibits IL-6 signal transduction by decreasing the phosphorylation levels of STAT3. This effect is associated with decreased expression of Jak2 at both mRNA and protein levels. Moreover, we showed that TGF-beta1 inhibits IL-6-induced expression of the cancer-associated gene MUC1. These observations demonstrated a novel interaction between TGF-beta1 and IL-6 signalling and suggested another mechanism of how defects in TGF-beta signalling, frequently associated with prostate pathologies, can contribute to the disruption of tissue homeostasis.},
note = {Place: England},
keywords = {Cell Line, Cell Proliferation, Epithelial Cells/*metabolism, Humans, Interleukin-6/*antagonists & inhibitors/pharmacology, Janus Kinase 2/genetics/*metabolism, Male, Mucin-1/metabolism, Phosphorylation, Prostate/cytology/enzymology/*metabolism, Prostatic Hyperplasia/enzymology/*metabolism, RNA, RNA Interference, Signal Transduction, Smad Proteins/metabolism, Small Interfering/metabolism, STAT3 Transcription Factor/*metabolism, Transforming Growth Factor beta1/*pharmacology},
pubstate = {published},
tppubtype = {article}
}