@CONFERENCE{MTMT:34154565,
	title = {Radiosensitizing effect of metal nanoparticles in combination with histone deacetylase inhibitors},
	url = {https://m2.mtmt.hu/api/publication/34154565},
	author = {Igaz, Nóra and Szőke, Krisztina and Bocz, Csenge and Kovács, Dávid and Rónavári, Andrea and Szabó, Emilia Rita and Polanek, Róbert and Buhala, Andrea and Vizler, Csaba and Tiszlavicz, László and Rázga, Zsolt and Hideghéty, Katalin and Kónya, Zoltán and Csontné Kiricsi, Mónika},
	booktitle = {FAMÉ 2023},
	unique-id = {34154565},
	year = {2023},
	pages = {75-76},
	orcid-numbers = {Igaz, Nóra/0000-0003-1580-4397; Rónavári, Andrea/0000-0001-7054-0975; Szabó, Emilia Rita/0000-0003-3611-2066; Polanek, Róbert/0000-0003-3645-8331; Tiszlavicz, László/0000-0003-1134-6587; Rázga, Zsolt/0000-0003-4717-8482; Hideghéty, Katalin/0000-0001-7080-2365; Kónya, Zoltán/0000-0002-9406-8596; Csontné Kiricsi, Mónika/0000-0002-8416-2052}
}

@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:31130654,
	title = {Synergistic Radiosensitization by Gold Nanoparticles and the Histone Deacetylase Inhibitor SAHA in 2D and 3D Cancer Cell Cultures},
	url = {https://m2.mtmt.hu/api/publication/31130654},
	author = {Igaz, Nóra and Szőke, Krisztina and Kovács, Dávid and Buhala, Andrea and Varga, Zoltán and Bélteky, Péter and Rázga, Zsolt and Tiszlavicz, László and Vizler, Csaba and Hideghéty, Katalin and Kónya, Zoltán and Csontné Kiricsi, Mónika},
	doi = {10.3390/nano10010158},
	journal-iso = {NANOMATERIALS-BASEL},
	journal = {NANOMATERIALS},
	volume = {10},
	unique-id = {31130654},
	year = {2020},
	eissn = {2079-4991},
	orcid-numbers = {Igaz, Nóra/0000-0003-1580-4397; Varga, Zoltán/0000-0001-8537-6282; Rázga, Zsolt/0000-0003-4717-8482; Hideghéty, Katalin/0000-0001-7080-2365; Kónya, Zoltán/0000-0002-9406-8596; Csontné Kiricsi, Mónika/0000-0002-8416-2052}
}

@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:2763894,
	title = {Besides neuro-imaging, the Thy1-YFP mouse could serve for visualizing experimental tumours, inflammation and wound-healing},
	url = {https://m2.mtmt.hu/api/publication/2763894},
	author = {Jósvay, Katalin and Winter, Zoltán and Katona, Róbert László and Pecze, László and Marton, Annamária and Buhala, Andrea and Szakonyi, Gerda and Oláh, Zoltán and Vizler, Csaba},
	doi = {10.1038/srep06776},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {4},
	unique-id = {2763894},
	issn = {2045-2322},
	abstract = {The B6.Cg-Tg(Thy1-YFP)16Jrs/J transgenic mouse strain, widely used to study neuronal development and regeneration, expresses the yellow fluorescent protein (YFP) in the peripheral nerves and the central nervous system under the control of regulatory sequences of the Thy1 gene. The Thy1 (CD90) cell surface glycoprotein is present on many cell types besides neurons, and is known to be involved in cell adhesion, migration and signal transduction. We hypothesized that Thy1-activating conditions could probably activate the truncated Thy1 regulatory sequences used in the Thy1-YFP construct, resulting in YFP transgene expression outside the nervous system. We demonstrated that the stroma of subcutaneous tumours induced by the injection of 4T1 or MC26 carcinoma cells into BALB/c(Thy1-YFP) mice, carrying the same construct, indeed expressed the YFP transgene. In the tumour mass, the yellow-green fluorescent stromal cells were clearly distinguishable from 4T1 carcinoma cells stably transfected with red fluorescent protein. Local inflammation induced by subcutaneous injection of complete Freund's adjuvant, as well as the experimental wound-healing milieu, also triggered YFP fluorescence in both the BALB/c(Thy1-YFP) and B6.Cg-Tg(Thy1-YFP)16Jrs/J mice, pointing to eventual overlapping pathways of wound-healing, inflammation and tumour growth.},
	year = {2014},
	eissn = {2045-2322},
	pages = {6776-6783},
	orcid-numbers = {Szakonyi, Gerda/0000-0002-4366-4283}
}

@article{MTMT:2341377,
	title = {Functionally important amino acid residues in the transient receptor potential vanilloid 1 (TRPV1) ion channel – an overview of the current mutational data},
	url = {https://m2.mtmt.hu/api/publication/2341377},
	author = {Winter, Zoltán and Buhala, Andrea and Ötvös, Ferenc and Jósvay, Katalin and Vizler, Csaba and Dombi, György and Szakonyi, Gerda and Oláh, Zoltán},
	doi = {10.1186/1744-8069-9-30},
	journal-iso = {MOL PAIN},
	journal = {MOLECULAR PAIN},
	volume = {9},
	unique-id = {2341377},
	issn = {1744-8069},
	year = {2013},
	eissn = {1744-8069},
	orcid-numbers = {Szakonyi, Gerda/0000-0002-4366-4283}
}