@article{MTMT:31873459,
	title = {Progesterone receptor membrane component 1 regulates lipid homeostasis and drives oncogenic signaling resulting in breast cancer progression (vol 22, 75, 2020)},
	url = {https://m2.mtmt.hu/api/publication/31873459},
	author = {Asperger, Hannah and Stamm, Nadia and Gierke, Berthold and Pawlak, Michael and Hofmann, Ute and Zanger, Ulrich M. and Marton, Annamária and Katona, Róbert László and Buhala, Andrea and Vizler, Csaba and Cieslik, Jan-Philipp and Kovacevic, Zaklina and Richardson, Des R. and Ruckhaeberle, Eugen and Niederacher, Dieter and Fehm, Tanja and Neubauer, Hans and Ludescher, Marina},
	doi = {10.1186/s13058-020-01383-7},
	journal-iso = {BREAST CANCER RES},
	journal = {BREAST CANCER RESEARCH},
	volume = {23},
	unique-id = {31873459},
	issn = {1465-5411},
	abstract = {An amendment to this paper has been published and can be accessed via the original article.},
	year = {2021},
	eissn = {1465-542X}
}

@article{MTMT:31397452,
	title = {Progesterone receptor membrane component 1 regulates lipid homeostasis and drives oncogenic signaling resulting in breast cancer progression},
	url = {https://m2.mtmt.hu/api/publication/31397452},
	author = {Asperger, Hannah and Stamm, Nadia and Gierke, Berthold and Pawlak, Michael and Hofmann, Ute and Zanger, Ulrich M. and Marton, Annamária and Katona, Róbert László and Buhala, Andrea and Vizler, Csaba and Cieslik, Jan-Philipp and Ruckhaeberle, Eugen and Niederacher, Dieter and Fehm, Tanja and Neubauer, Hans and Ludescher, Marina},
	doi = {10.1186/s13058-020-01312-8},
	journal-iso = {BREAST CANCER RES},
	journal = {BREAST CANCER RESEARCH},
	volume = {22},
	unique-id = {31397452},
	issn = {1465-5411},
	abstract = {Background: PGRMC1 (progesterone receptor membrane component 1) is a highly conserved heme binding protein, which is overexpressed especially in hormone receptor-positive breast cancer and plays an important role in breast carcinogenesis. Nevertheless, little is known about the mechanisms by which PGRMC1 drives tumor progression. The aim of our study was to investigate the involvement of PGRMC1 in cholesterol metabolism to detect new mechanisms by which PGRMC1 can increase lipid metabolism and alter cancer-related signaling pathways leading to breast cancer progression. Methods: The effect of PGRMC1 overexpression and silencing on cellular proliferation was examined in vitro and in a xenograft mouse model. Next, we investigated the interaction of PGRMC1 with enzymes involved in the cholesterol synthesis pathway such as CYP51, FDFT1, and SCD1. Further, the impact of PGRMC1 expression on lipid levels and expression of enzymes involved in lipid homeostasis was examined. Additionally, we assessed the role of PGRMC1 in key cancer-related signaling pathways including EGFR/HER2 and ER alpha signaling. Results: Overexpression of PGRMC1 resulted in significantly enhanced proliferation. PGRMC1 interacted with key enzymes of the cholesterol synthesis pathway, alters the expression of proteins, and results in increased lipid levels. PGRMC1 also influenced lipid raft formation leading to altered expression of growth receptors in membranes of breast cancer cells. Analysis of activation of proteins revealed facilitated ER alpha and EGFR activation and downstream signaling dependent on PGRMC1 overexpression in hormone receptor-positive breast cancer cells. Depletion of cholesterol and fatty acids induced by statins reversed this growth benefit. Conclusion: PGRMC1 may mediate proliferation and progression of breast cancer cells potentially by altering lipid metabolism and by activating key oncogenic signaling pathways, such as ER alpha expression and activation, as well as EGFR signaling. Our present study underlines the potential of PGRMC1 as a target for anti-cancer therapy.},
	year = {2020},
	eissn = {1465-542X}
}

@article{MTMT:31183285,
	title = {Polyploid Adipose Stem Cells Shift the Balance of IGF1/IGFBP2 to Promote the Growth of Breast Cancer},
	url = {https://m2.mtmt.hu/api/publication/31183285},
	author = {Fajka-Boja, Roberta and Szebeni, Gábor and Hunyadi-Gulyás Éva, Csilla and Puskás, László and Katona, Róbert László},
	doi = {10.3389/fonc.2020.00157},
	journal-iso = {FRONT ONCOL},
	journal = {FRONTIERS IN ONCOLOGY},
	volume = {10},
	unique-id = {31183285},
	issn = {2234-943X},
	year = {2020},
	eissn = {2234-943X},
	orcid-numbers = {Szebeni, Gábor/0000-0002-6998-5632}
}

@article{MTMT:30898978,
	title = {Melanoma-Derived Exosomes Induce PD-1 Overexpression and Tumor Progression via Mesenchymal Stem Cell Oncogenic Reprogramming},
	url = {https://m2.mtmt.hu/api/publication/30898978},
	author = {Gyukity-Sebestyén, Edina and Harmati, Mária and Dobra, Gabriella and Németh, István Balázs and Mihály, Johanna and Zvara, Ágnes and Hunyadi-Gulyás Éva, Csilla and Katona, Róbert László and Nagy, István and Horváth, Péter and Bálind, Árpád and Szkalisity, Ábel and Kovács, Mária and Pankotai, Tibor and Borsos, Barbara Nikolett and Erdélyi, Miklós and Szegletes, Zsolt and Veréb, Zoltán and Buzás, Edit Irén and Kemény, Lajos and Bíró, Tamás and Buzás, Krisztina},
	doi = {10.3389/fimmu.2019.02459},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {10},
	unique-id = {30898978},
	issn = {1664-3224},
	abstract = {Recently, it has been described that programmed cell death protein 1 (PD-1) overexpressing melanoma cells are highly aggressive. However, until now it has not been defined which factors lead to the generation of PD-1 overexpressing subpopulations. Here, we present that melanoma-derived exosomes, conveying oncogenic molecular reprogramming, induce the formation of a melanoma-like, PD-1 overexpressing cell population (mMSCPD-1+) from naïve mesenchymal stem cells (MSCs). Exosomes and mMSCPD-1+ cells induce tumor progression and expression of oncogenic factors in vivo. Finally, we revealed a characteristic, tumorigenic signaling network combining the upregulated molecules (e.g., PD-1, MET, RAF1, BCL2, MTOR) and their upstream exosomal regulating proteins and miRNAs. Our study highlights the complexity of exosomal communication during tumor progression and contributes to the detailed understanding of metastatic processes.},
	keywords = {METASTASIS; stem cell; exosome; Reprogramming; PD-1; melanoma/tumor progression; signalization pattern},
	year = {2019},
	eissn = {1664-3224},
	orcid-numbers = {Gyukity-Sebestyén, Edina/0000-0003-1383-6301; Harmati, Mária/0000-0002-4875-5723; Dobra, Gabriella/0000-0002-2814-7720; Pankotai, Tibor/0000-0001-9810-5465; Erdélyi, Miklós/0000-0002-9501-5752; Szegletes, Zsolt/0000-0003-2202-6933; Veréb, Zoltán/0000-0002-9518-2155; Buzás, Edit Irén/0000-0002-3744-206X; Kemény, Lajos/0000-0002-2119-9501; Buzás, Krisztina/0000-0001-8933-2033}
}

@article{MTMT:30693937,
	title = {Adipose stem cells may promote cancer progression},
	url = {https://m2.mtmt.hu/api/publication/30693937},
	author = {Fajka-Boja, Roberta and Marton, Annamária and Tóth, Anna and Blazsó, Péter and Tubak, Vilmos and Bálint, Balázs and Nagy, István and Hegedűs, Zoltán and Vizler, Csaba and Katona, Róbert László},
	doi = {10.32907/RO-106-110113},
	journal-iso = {RO},
	journal = {RESEARCH OUTREACH},
	volume = {2019},
	unique-id = {30693937},
	issn = {2517-701X},
	year = {2019},
	eissn = {2517-7028},
	pages = {6-9},
	orcid-numbers = {Blazsó, Péter/0000-0003-4404-8068; Tubak, Vilmos/0000-0002-6141-3920}
}

@article{MTMT:3411662,
	title = {Increased insulin-like growth factor 1 production by polyploid adipose stem cells promotes growth of breast cancer cells},
	url = {https://m2.mtmt.hu/api/publication/3411662},
	author = {Fajka-Boja, Roberta and Marton, Annamária and Tóth, Anna and Blazsó, Péter and Tubak, Vilmos and Bálint, Balázs and Nagy, István and Hegedűs, Zoltán and Vizler, Csaba and Katona, Róbert László},
	doi = {10.1186/s12885-018-4781-z},
	journal-iso = {BMC CANCER},
	journal = {BMC CANCER},
	volume = {18},
	unique-id = {3411662},
	issn = {1471-2407},
	year = {2018},
	eissn = {1471-2407},
	orcid-numbers = {Blazsó, Péter/0000-0003-4404-8068; Tubak, Vilmos/0000-0002-6141-3920}
}

@article{MTMT:3250677,
	title = {Targeting breast cancer cells by MRS1477, a positive allosteric modulator of TRPV1 channels},
	url = {https://m2.mtmt.hu/api/publication/3250677},
	author = {Naziroglu, M and Cig, B and Blum, W and Vizler, Csaba and Buhala, Andrea and Marton, Annamária and Katona, Róbert László and Jósvay, Katalin and Schwaller, B and Oláh, Zoltán and Pecze, László},
	doi = {10.1371/journal.pone.0179950},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {12},
	unique-id = {3250677},
	issn = {1932-6203},
	abstract = {There is convincing epidemiological and experimental evidence that capsaicin, a potent natural transient receptor potential cation channel vanilloid member 1 (TRPV1) agonist, has anticancer activity. However, capsaicin cannot be given systemically in large doses, because of its induction of acute pain and neurological inflammation. MRS1477, a dihydropyridine derivative acts as a positive allosteric modulator of TRPV1, if added together with capsaicin, but is ineffective, if given alone. Addition of MRS1477 evoked Ca2+ signals in MCF7 breast cancer cells, but not in primary breast epithelial cells. This indicates that MCF7 cells not only express functional TRPV1 channels, but also produce endogenous TRPV1 agonists. We investigated the effects of MRS1477 and capsaicin on cell viability, caspase-3 and -9 activities and reactive oxygen species production in MCF7 cells. The fraction of apoptotic cells was increased after 3 days incubation with capsaicin (10 mu M) paralleled by increased reactive oxygen species production and caspase activity. These effects were even more pronounced, when cells were incubated with MRS1477 (2 mu M) either alone or together with CAPS (10 mu M). Capsazepine, a TRPV1 blocker, inhibited both the effect of capsaicin and MRS1477. Whole-cell patch clamp recordings revealed that capsaicinevoked TRPV1-mediated current density levels were increased after 3 days incubation with MRS1477 (2 mu M). However, the tumor growth in MCF7 tumor-bearing immunodeficient mice was not significantly decreased after treatment with MRS1477 (10 mg/kg body weight, i.p., injection twice a week). In conclusion, in view of a putative in vivo treatment with MRS1477 or similar compounds further optimization is required.},
	year = {2017},
	eissn = {1932-6203}
}

@article{MTMT:2995020,
	title = {Bacterial sepsis increases survival in metastatic melanoma: Chlamydophila pneumoniae induces macrophage polarization and tumor regression},
	url = {https://m2.mtmt.hu/api/publication/2995020},
	author = {Buzás, Krisztina and Marton, Annamária and Vizler, Csaba and Gyukity-Sebestyén, Edina and Harmati, Mária and Nagy, Katalin and Zvara, Ágnes and Katona, Róbert László and Tubak, Vilmos and Endrész, Valéria and Németh, István Balázs and Oláh, Judit Magdolna and Vigh, László and Bíró, Tamás and Kemény, Lajos},
	doi = {10.1016/j.jid.2015.12.032},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	volume = {136},
	unique-id = {2995020},
	issn = {0022-202X},
	year = {2016},
	eissn = {1523-1747},
	pages = {862-865},
	orcid-numbers = {Buzás, Krisztina/0000-0001-8933-2033; Gyukity-Sebestyén, Edina/0000-0003-1383-6301; Harmati, Mária/0000-0002-4875-5723; Nagy, Katalin/0000-0001-9383-5952; Tubak, Vilmos/0000-0002-6141-3920; Endrész, Valéria/0000-0002-9402-3857; Kemény, Lajos/0000-0002-2119-9501}
}

@article{MTMT:2946565,
	title = {Licensing by Inflammatory Cytokines Abolishes Heterogeneity of Immunosuppressive Function of Mesenchymal Stem Cell Population},
	url = {https://m2.mtmt.hu/api/publication/2946565},
	author = {Szabó, Enikő and Fajka-Boja, Roberta and Kriston-Pál, Éva and Hornung, Ákos and Makra, Ildikó and Kudlik, Gyöngyi and Uher, Ferenc and Katona, Róbert László and Monostori, Éva and Czibula, Ágnes},
	doi = {10.1089/scd.2014.0581},
	journal-iso = {STEM CELLS DEV},
	journal = {STEM CELLS AND DEVELOPMENT},
	volume = {24},
	unique-id = {2946565},
	issn = {1547-3287},
	abstract = {When mesenchymal stem cells (MSCs) are used for therapy of immunological pathologies, they get into an inflammatory environment, altering the effectiveness of the treatment. To establish the impact of environmental inflammatory factors on MSCs' immunofunction in the mirror of intrinsic heterogeneity of mouse MSC population, individual MSC clones were generated and characterized. Adipogenic but not osteogenic differentiation and pro-angiogenic activity of five independent MSC cell lines were similar. Regarding osteogenic differentiation, clones MSC3 and MSC6 exhibited poorer capacity than MSC2, MSC4, and MSC5. To study the immunosuppressive heterogeneity, in vitro and in vivo experiments have been carried out using T-cell proliferation assay and delayed-type hypersensitivity (DTH) response, respectively. A remarkable difference was found between the clones in their ability to inhibit T-cell proliferation in the following order: MSC2MSC5>MSC4>MSC3>>MSC6. Nevertheless, the differences between the immunosuppressive activities of the individual clones disappeared on pretreatment of the cells with pro-inflammatory cytokines, a procedure called licensing. Stimulation of all clones with IFN- and TNF- resulted in elevation of their inhibitory capability to a similar level. Nitric oxide (NO) and prostaglandin E2 (PGE2) were identified as major mediators of immunofunction of the MSC clones. The earlier findings were also supported by in vivo results. Without licensing, MSC2 inhibited DTH response, while MSC6 did not affect DTH response. In contrast, prestimulation of MSC6 with inflammatory cytokines resulted in strong suppression by this clone as well. Here, we have showed that MSC population is functionally heterogeneous in terms of immunosuppressive function; however, this variability is largely reduced under pro-inflammatory conditions.},
	year = {2015},
	eissn = {1557-8534},
	pages = {2171-2180},
	orcid-numbers = {Uher, Ferenc/0000-0001-7997-6142; Monostori, Éva/0000-0002-7442-3562}
}

@article{MTMT:2897512,
	title = {Human artificial chromosomes for future biomedicine.},
	url = {https://m2.mtmt.hu/api/publication/2897512},
	author = {Katona, Róbert László},
	doi = {10.1080/15384101.2015.1032647},
	journal-iso = {CELL CYCLE},
	journal = {CELL CYCLE},
	volume = {14},
	unique-id = {2897512},
	issn = {1538-4101},
	year = {2015},
	eissn = {1551-4005},
	pages = {1494-1494}
}