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Article ; Online: High-Throughput, Parallel Flow Cytometry Screening of Hundreds of Cell Surface Antigens Using Fluorescent Barcoding.

Drápela, Stanislav / Fedr, Radek / Vacek, Ondřej / Remšík, Ján / Souček, Karel

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2543, Page(s) 99–111

Abstract: Multicolor flow cytometry allows for analysis of tens of cellular parameters in millions of cells at a single-cell resolution within minutes. The lack of technologies that would facilitate feasible and relatively cheap profiling of such a number of cells ...

Abstract	Multicolor flow cytometry allows for analysis of tens of cellular parameters in millions of cells at a single-cell resolution within minutes. The lack of technologies that would facilitate feasible and relatively cheap profiling of such a number of cells with an antibody-based approach led us to the development of a high-throughput cytometry-based platform for surface profiling. We coupled the fluorescent cell barcoding with preexisting, commercially available screening tools to analyze cell surface fingerprint at a large scale. This powerful approach will help to identify novel biomarkers and druggable targets and facilitate the discovery of new concepts in immunology, oncology, and developmental biology.
MeSH term(s)	Antigens, Surface ; Biomarkers/analysis ; Flow Cytometry ; Fluorescent Dyes ; Research
Chemical Substances	Antigens, Surface ; Biomarkers ; Fluorescent Dyes
Language	English
Publishing date	2022-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2553-8_9
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Article ; Online: TGF-β regulates Sca-1 expression and plasticity of pre-neoplastic mammary epithelial stem cells.

Remšík, Ján / Pícková, Markéta / Vacek, Ondřej / Fedr, Radek / Binó, Lucia / Hampl, Aleš / Souček, Karel

Scientific reports

2020 Volume 10, Issue 1, Page(s) 11396

Abstract: The epithelial-mesenchymal plasticity, in tight association with stemness, contributes to the mammary gland homeostasis, evolution of early neoplastic lesions and cancer dissemination. Focused on cell surfaceome, we used mouse models of pre-neoplastic ... ...

Abstract	The epithelial-mesenchymal plasticity, in tight association with stemness, contributes to the mammary gland homeostasis, evolution of early neoplastic lesions and cancer dissemination. Focused on cell surfaceome, we used mouse models of pre-neoplastic mammary epithelial and cancer stem cells to reveal the connection between cell surface markers and distinct cell phenotypes. We mechanistically dissected the TGF-β family-driven regulation of Sca-1, one of the most commonly used adult stem cell markers. We further provided evidence that TGF-β disrupts the lineage commitment and promotes the accumulation of tumor-initiating cells in pre-neoplastic cells.
MeSH term(s)	Animals ; Ataxin-1/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor/transplantation ; Cell Plasticity/genetics ; Epithelial Cells/pathology ; Epithelial-Mesenchymal Transition/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mammary Glands, Animal/pathology ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/pathology ; Mice ; Neoplastic Stem Cells/pathology ; Receptor, ErbB-2/genetics ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Signal Transduction/genetics ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Ataxin-1 ; Atxn1 protein, mouse ; Recombinant Proteins ; Transforming Growth Factor beta ; Erbb2 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2020-07-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-67827-4
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Article ; Online: Skp2 and Slug Are Coexpressed in Aggressive Prostate Cancer and Inhibited by Neddylation Blockade.

Mickova, Alena / Kharaishvili, Gvantsa / Kurfurstova, Daniela / Gachechiladze, Mariam / Kral, Milan / Vacek, Ondrej / Pokryvkova, Barbora / Mistrik, Martin / Soucek, Karel / Bouchal, Jan

International journal of molecular sciences

2021 Volume 22, Issue 6

Abstract: Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men in Western countries, and there is still an urgent need for a better understanding of PCa progression to inspire new treatment strategies. Skp2 is a substrate-recruiting ... ...

Abstract	Prostate cancer (PCa) is the second leading cause of cancer-related deaths in men in Western countries, and there is still an urgent need for a better understanding of PCa progression to inspire new treatment strategies. Skp2 is a substrate-recruiting component of the E3 ubiquitin ligase complex, whose activity is regulated through neddylation. Slug is a transcriptional repressor involved in the epithelial-to-mesenchymal transition, which may contribute to therapy resistance. Although Skp2 has previously been associated with a mesenchymal phenotype and prostate cancer progression, the relationship with Slug deserves further elucidation. We have previously shown that a high Gleason score (≥8) is associated with higher Skp2 and lower E-cadherin expression. In this study, significantly increased expression of Skp2, AR, and Slug, along with E-cadherin downregulation, was observed in primary prostate cancer in patients who already had lymph node metastases. Skp2 was slightly correlated with Slug and AR in the whole cohort (Rs 0.32 and 0.37, respectively), which was enhanced for both proteins in patients with high Gleason scores (Rs 0.56 and 0.53, respectively) and, in the case of Slug, also in patients with metastasis to lymph nodes (Rs 0.56). Coexpression of Skp2 and Slug was confirmed in prostate cancer tissues by multiplex immunohistochemistry and confocal microscopy. The same relationship between these two proteins was observed in three sets of prostate epithelial cell lines (PC3, DU145, and E2) and their mesenchymal counterparts. Chemical inhibition of Skp2, but not RNA interference, modestly decreased Slug protein in PC3 and its docetaxel-resistant subline PC3 DR12. Importantly, chemical inhibition of Skp2 by MLN4924 upregulated p27 and decreased Slug expression in PC3, PC3 DR12, and LAPC4 cells. Novel treatment strategies targeting Skp2 and Slug by the neddylation blockade may be promising in advanced prostate cancer, as recently documented for other aggressive solid tumors.
MeSH term(s)	Antigens, CD/genetics ; Antigens, CD/metabolism ; Antineoplastic Agents/pharmacology ; Cadherins/genetics ; Cadherins/metabolism ; Cell Line, Tumor ; Cell Survival/drug effects ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Cyclopentanes/pharmacology ; Docetaxel/pharmacology ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphatic Metastasis ; Male ; NEDD8 Protein/genetics ; NEDD8 Protein/metabolism ; Neoplasm Grading ; PC-3 Cells ; Prostate/metabolism ; Prostate/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Processing, Post-Translational ; Pyrimidines/pharmacology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors ; S-Phase Kinase-Associated Proteins/genetics ; S-Phase Kinase-Associated Proteins/metabolism ; Snail Family Transcription Factors/genetics ; Snail Family Transcription Factors/metabolism
Chemical Substances	Antigens, CD ; Antineoplastic Agents ; CDH1 protein, human ; Cadherins ; Cyclopentanes ; NEDD8 Protein ; NEDD8 protein, human ; Pyrimidines ; RNA, Small Interfering ; Receptors, Androgen ; S-Phase Kinase-Associated Proteins ; SKP2 protein, human ; SNAI1 protein, human ; Snail Family Transcription Factors ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Docetaxel (15H5577CQD) ; pevonedistat (S3AZD8D215)
Language	English
Publishing date	2021-03-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22062844
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Article ; Online: TACSTD2 upregulation is an early reaction to lung infection.

Lenárt, Sára / Lenárt, Peter / Knopfová, Lucia / Kotasová, Hana / Pelková, Vendula / Sedláková, Veronika / Vacek, Ondřej / Pokludová, Jana / Čan, Vladimír / Šmarda, Jan / Souček, Karel / Hampl, Aleš / Beneš, Petr

Scientific reports

2022 Volume 12, Issue 1, Page(s) 9583

Abstract: TACSTD2 encodes a transmembrane glycoprotein Trop2 commonly overexpressed in carcinomas. While the Trop2 protein was discovered already in 1981 and first antibody-drug conjugate targeting Trop2 were recently approved for cancer therapy, the physiological ...

Abstract	TACSTD2 encodes a transmembrane glycoprotein Trop2 commonly overexpressed in carcinomas. While the Trop2 protein was discovered already in 1981 and first antibody-drug conjugate targeting Trop2 were recently approved for cancer therapy, the physiological role of Trop2 is still not fully understood. In this article, we show that TACSTD2/Trop2 expression is evolutionarily conserved in lungs of various vertebrates. By analysis of publicly available transcriptomic data we demonstrate that TACSTD2 level consistently increases in lungs infected with miscellaneous, but mainly viral pathogens. Single cell and subpopulation based transcriptomic data revealed that the major source of TACSTD2 transcript are lung epithelial cells and their progenitors and that TACSTD2 is induced directly in lung epithelial cells following infection. Increase in TACSTD2 expression may represent a mechanism to maintain/restore epithelial barrier function and contribute to regeneration process in infected/damaged lungs.
MeSH term(s)	Animals ; Antigens, Neoplasm/metabolism ; Cell Adhesion Molecules/metabolism ; Epithelial Cells/metabolism ; Lung/metabolism ; Up-Regulation
Chemical Substances	Antigens, Neoplasm ; Cell Adhesion Molecules
Language	English
Publishing date	2022-06-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-13637-9
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Article: A prolonged exposure of human lung carcinoma epithelial cells to benzo[a]pyrene induces p21-dependent epithelial-to-mesenchymal transition (EMT)-like phenotype

Hýžďalová, Martina / Procházková, Jiřina / Strapáčová, Simona / Svržková, Lucie / Vacek, Ondřej / Fedr, Radek / Andrysík, Zdeněk / Hrubá, Eva / Líbalová, Helena / Kléma, Jiří / Topinka, Jan / Mašek, Josef / Souček, Karel / Vondráček, Jan / Machala, Miroslav

Chemosphere. 2021 Jan., v. 263

2021

Abstract: Deciphering the role of the aryl hydrocarbon receptor (AhR) in lung cancer cells may help us to better understand the role of toxic AhR ligands in lung carcinogenesis, including cancer progression. We employed human lung carcinoma A549 cells to ... ...

Abstract	Deciphering the role of the aryl hydrocarbon receptor (AhR) in lung cancer cells may help us to better understand the role of toxic AhR ligands in lung carcinogenesis, including cancer progression. We employed human lung carcinoma A549 cells to investigate their fate after continuous two-week exposure to model AhR agonists, genotoxic benzo[a]pyrene (BaP; 1 μM) and non-genotoxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 10 nM). While TCDD increased proliferative rate of A549 cells, exposure to BaP decreased cell proliferation and induced epithelial-to-mesenchymal transition (EMT)-like phenotype, which was associated with enhanced cell migration, invasion, and altered cell morphology. Although TCDD also suppressed expression of E-cadherin and activated some genes linked to EMT, it did not induce the EMT-like phenotype. The results of transcriptomic analysis, and the opposite effects of BaP and TCDD on cell proliferation, indicated that a delay in cell cycle progression, together with a slight increase of senescence (when coupled with AhR activation), favors the induction of EMT-like phenotype. The shift towards EMT-like phenotype observed after simultaneous treatment with TCDD and mitomycin C (an inhibitor of cell proliferation) confirmed the hypothesis. Since BaP decreased cell proliferative rate via induction of p21 expression, we generated the A549 cell model with reduced p21 expression and exposed it to BaP for two weeks. The p21 knockdown suppressed the BaP-mediated EMT-like phenotype in A549 cells, thus confirming that a delayed cell cycle progression, together with p21-dependent induction of senescence-related chemokine CCL2, may contribute to induction of EMT-like cell phenotype in lung cells exposed to genotoxic AhR ligands.
Keywords	aryl hydrocarbon receptors ; cadherins ; carcinogenesis ; cell cycle ; cell movement ; cell proliferation ; cell structures ; chemokine CCL2 ; epithelium ; humans ; ligands ; lung neoplasms ; lungs ; mitomycin ; models ; mutagens ; neoplasm progression ; phenotype ; tetrachlorodibenzo-p-dioxin ; toxicity ; transcriptomics
Language	English
Dates of publication	2021-01
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-light
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2020.128126
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A prolonged exposure of human lung carcinoma epithelial cells to benzo[a]pyrene induces p21-dependent epithelial-to-mesenchymal transition (EMT)-like phenotype.

Chemosphere

2020 Volume 263, Page(s) 128126

Abstract	Deciphering the role of the aryl hydrocarbon receptor (AhR) in lung cancer cells may help us to better understand the role of toxic AhR ligands in lung carcinogenesis, including cancer progression. We employed human lung carcinoma A549 cells to investigate their fate after continuous two-week exposure to model AhR agonists, genotoxic benzo[a]pyrene (BaP; 1 μM) and non-genotoxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 10 nM). While TCDD increased proliferative rate of A549 cells, exposure to BaP decreased cell proliferation and induced epithelial-to-mesenchymal transition (EMT)-like phenotype, which was associated with enhanced cell migration, invasion, and altered cell morphology. Although TCDD also suppressed expression of E-cadherin and activated some genes linked to EMT, it did not induce the EMT-like phenotype. The results of transcriptomic analysis, and the opposite effects of BaP and TCDD on cell proliferation, indicated that a delay in cell cycle progression, together with a slight increase of senescence (when coupled with AhR activation), favors the induction of EMT-like phenotype. The shift towards EMT-like phenotype observed after simultaneous treatment with TCDD and mitomycin C (an inhibitor of cell proliferation) confirmed the hypothesis. Since BaP decreased cell proliferative rate via induction of p21 expression, we generated the A549 cell model with reduced p21 expression and exposed it to BaP for two weeks. The p21 knockdown suppressed the BaP-mediated EMT-like phenotype in A549 cells, thus confirming that a delayed cell cycle progression, together with p21-dependent induction of senescence-related chemokine CCL2, may contribute to induction of EMT-like cell phenotype in lung cells exposed to genotoxic AhR ligands.
MeSH term(s)	Benzo(a)pyrene/toxicity ; Carcinoma ; Epithelial Cells ; Humans ; Lung ; Lung Neoplasms/genetics ; Phenotype ; Receptors, Aryl Hydrocarbon/genetics
Chemical Substances	Receptors, Aryl Hydrocarbon ; Benzo(a)pyrene (3417WMA06D)
Language	English
Publishing date	2020-09-10
Publishing country	England
Document type	Journal Article
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2020.128126
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Article ; Online: Toll-Like Receptor 3 Overexpression Induces Invasion of Prostate Cancer Cells, whereas Its Activation Triggers Apoptosis.

Muresan, Ximena M / Slabáková, Eva / Procházková, Jiřina / Drápela, Stanislav / Fedr, Radek / Pícková, Markéta / Vacek, Ondřej / Víchová, Ráchel / Suchánková, Tereza / Bouchal, Jan / Kürfürstová, Daniela / Král, Milan / Hulínová, Tereza / Sýkora, Radek P / Študent, Vladimír / Hejret, Václav / van Weerden, Wytske M / Puhr, Martin / Pustka, Václav /

Potěšil, David / Zdráhal, Zbyněk / Culig, Zoran / Souček, Karel

The American journal of pathology

2022 Volume 192, Issue 9, Page(s) 1321–1335

Abstract: Toll-like receptor 3 (TLR3) is an endosomal receptor expressed in several immune and epithelial cells. Recent studies have highlighted its expression also in solid tumors, including prostate cancer (PCa), and have described its role primarily in the ... ...

Abstract	Toll-like receptor 3 (TLR3) is an endosomal receptor expressed in several immune and epithelial cells. Recent studies have highlighted its expression also in solid tumors, including prostate cancer (PCa), and have described its role primarily in the proinflammatory response and induction of apoptosis. It is up-regulated in some castration-resistant prostate cancers. However, the role of TLR3 in prostate cancer progression remains largely unknown. The current study experimentally demonstrated that exogenous TLR3 activation in PCa cell lines leads to a significant induction of secretion of the cytokines IL-6, IL-8, and interferon-β, depending on the model and chemoresistance status. Transcriptomic analysis of TLR3-overexpressing cells revealed a functional program that is enriched for genes involved in the regulation of cell motility, migration, and tumor invasiveness. Increased motility, migration, and invasion in TLR3-overexpressing cell line were confirmed by several in vitro assays and using an orthotopic prostate xenograft model in vivo. Furthermore, TLR3-ligand induced apoptosis via cleavage of caspase-3/7 and poly (ADP-ribose) polymerase, predominantly in TLR3-overexpressing cells. These results indicate that TLR3 may be involved in prostate cancer progression and metastasis; however, it might also represent an Achilles heel of PCa, which can be exploited for targeted therapy.
MeSH term(s)	Animals ; Apoptosis ; Cell Line, Tumor ; Humans ; Male ; Poly I-C/pharmacology ; Prostate/pathology ; Prostatic Neoplasms/pathology ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/metabolism
Chemical Substances	TLR3 protein, human ; Toll-Like Receptor 3 ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2022.05.009
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Article ; Online: High-Throughput, Parallel Flow Cytometry Screening of Hundreds of Cell Surface Antigens Using Fluorescent Barcoding.

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Article ; Online: TGF-β regulates Sca-1 expression and plasticity of pre-neoplastic mammary epithelial stem cells.

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Article ; Online: Skp2 and Slug Are Coexpressed in Aggressive Prostate Cancer and Inhibited by Neddylation Blockade.

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Article ; Online: TACSTD2 upregulation is an early reaction to lung infection.

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Article: A prolonged exposure of human lung carcinoma epithelial cells to benzo[a]pyrene induces p21-dependent epithelial-to-mesenchymal transition (EMT)-like phenotype

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Article ; Online: A prolonged exposure of human lung carcinoma epithelial cells to benzo[a]pyrene induces p21-dependent epithelial-to-mesenchymal transition (EMT)-like phenotype.

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Article ; Online: Toll-Like Receptor 3 Overexpression Induces Invasion of Prostate Cancer Cells, whereas Its Activation Triggers Apoptosis.

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