@article{MTMT:34820104,
	title = {Quantifying antibody-dependent cellular cytotoxicity in a tumor spheroid model : application for drug discovery},
	url = {https://m2.mtmt.hu/api/publication/34820104},
	author = {Isotta, Sturniolo and Csongor, Váróczy and Ákos, Máté Bede and Hegedűs, Csaba and Demény, Máté Ágoston and Virág, László},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	unique-id = {34820104},
	issn = {1940-087X},
	year = {2024},
	eissn = {1940-087X}
}

@article{MTMT:34754751,
	title = {PARP14 contributes to the development of the tumor-associated macrophage phenotype},
	url = {https://m2.mtmt.hu/api/publication/34754751},
	author = {Sturniolo, I and Váróczy, Cs and Regdon, Zsolt and Mázló, A and Muzsai, Sz and Bácsi, A and Intili, G and Hegedűs, Csaba and Boothby, MR and Holechek, J and Ferraris, D and Schüler, H and Virág, László},
	doi = {10.3390/ijms25073601},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34754751},
	issn = {1661-6596},
	year = {2024},
	eissn = {1422-0067},
	pages = {1-21}
}

@article{MTMT:34729573,
	title = {Automated high-throughput cell culture scratch assay identifies wound healing promoting and inhibiting compounds from a small compound library of redox active molecules},
	url = {https://m2.mtmt.hu/api/publication/34729573},
	author = {Virág, László and Hegedűs, Csaba and Kovács, Katalin and Polgár, Zsuzsanna and Kókai, Endre and Sturniolo, Isotta and Demény, Máté Ágoston and Virág, Bernadett and Szabó, Éva},
	doi = {10.1016/j.freeradbiomed.2023.10.328},
	journal-iso = {FREE RADICAL BIO MED},
	journal = {FREE RADICAL BIOLOGY AND MEDICINE},
	volume = {208},
	unique-id = {34729573},
	issn = {0891-5849},
	year = {2023},
	eissn = {1873-4596},
	pages = {S144-S144}
}

@article{MTMT:34108111,
	title = {High-Content Screening Assay for the Identification of Antibody-Dependent Cellular Cytotoxicity Modifying Compounds},
	url = {https://m2.mtmt.hu/api/publication/34108111},
	author = {Guti, Eliza and Bede, Ákos Máté and Váróczy, Csongor and Hegedűs, Csaba and Demény, Máté Ágoston and Virág, László},
	doi = {10.3791/64485},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	unique-id = {34108111},
	issn = {1940-087X},
	year = {2023},
	eissn = {1940-087X},
	pages = {1-12}
}

@article{MTMT:34089348,
	title = {Identification of Bacterial Metabolites Modulating Breast Cancer Cell Proliferation and Epithelial-Mesenchymal Transition},
	url = {https://m2.mtmt.hu/api/publication/34089348},
	author = {Ujlaki, Gyula and Kovács, Tünde and Vida, András and Kókai, Endre and Rauch, Boglárka and Schwarcz, Szandra and Mikó, Edit and Janka, Eszter and Sipos, Adrienn and Hegedűs, Csaba and Uray (Davis), Karen L. and Nagy, Péter and Bay, Péter},
	doi = {10.3390/molecules28155898},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {28},
	unique-id = {34089348},
	issn = {1420-3049},
	abstract = {Breast cancer patients are characterized by the oncobiotic transformation of multiple microbiome communities, including the gut microbiome. Oncobiotic transformation of the gut microbiome impairs the production of antineoplastic bacterial metabolites. The goal of this study was to identify bacterial metabolites with antineoplastic properties. We constructed a 30-member bacterial metabolite library and screened the library compounds for effects on cell proliferation and epithelial-mesenchymal transition. The metabolites were applied to 4T1 murine breast cancer cells in concentrations corresponding to the reference serum concentrations. However, yric acid, glycolic acid, d-mannitol, 2,3-butanediol, and trans-ferulic acid exerted cytostatic effects, and 3-hydroxyphenylacetic acid, 4-hydroxybenzoic acid, and vanillic acid exerted hyperproliferative effects. Furthermore, 3-hydroxyphenylacetic acid, 4-hydroxybenzoic acid, 2,3-butanediol, and hydrocinnamic acid inhibited epithelial-to-mesenchymal (EMT) transition. We identified redox sets among the metabolites (d-mannitol—d-mannose, 1-butanol—butyric acid, ethylene glycol—glycolic acid—oxalic acid), wherein only one partner within the set (d-mannitol, butyric acid, glycolic acid) possessed bioactivity in our system, suggesting that changes to the local redox potential may affect the bacterial secretome. Of the nine bioactive metabolites, 2,3-butanediol was the only compound with both cytostatic and anti-EMT properties.},
	year = {2023},
	eissn = {1420-3049},
	orcid-numbers = {Janka, Eszter/0000-0003-0724-5281; Nagy, Péter/0000-0002-7466-805X}
}

@article{MTMT:34082035,
	title = {Migration of Myogenic Cells Is Highly Influenced by Cytoskeletal Septin7},
	url = {https://m2.mtmt.hu/api/publication/34082035},
	author = {Ráduly, Zsolt and Szabó, László and Dienes, Beatrix and Szentesi, Péter and Bana, Ágnes Viktória and Hajdú, Tibor and Kókai, Endre and Hegedűs, Csaba and Csernoch, László and Gönczi, Mónika},
	doi = {10.3390/cells12141825},
	journal-iso = {CELLS-BASEL},
	journal = {CELLS},
	volume = {12},
	unique-id = {34082035},
	abstract = {Septin7 as a unique member of the GTP binding protein family, is widely expressed in the eukaryotic cells and considered to be essential in the formation of hetero-oligomeric septin complexes. As a cytoskeletal component, Septin7 is involved in many important cellular processes. However, its contribution in striated muscle physiology is poorly described. In skeletal muscle, a highly orchestrated process of migration is crucial in the development of functional fibers and in regeneration. Here, we describe the pronounced appearance of Septin7 filaments and a continuous change of Septin7 protein architecture during the migration of myogenic cells. In Septin7 knockdown C2C12 cultures, the basic parameters of migration are significantly different, and the intracellular calcium concentration change in migrating cells are lower compared to that of scrambled cultures. Using a plant cytokinin, forchlorfenuron, to dampen septin dynamics, the altered behavior of the migrating cells is described, where Septin7-depleted cells are more resistant to the treatment. These results indicate the functional relevance of Septin7 in the migration of myoblasts, implying its contribution to muscle myogenesis and regeneration.},
	keywords = {INTRACELLULAR CALCIUM; regeneration; CYTOSKELETON; myogenesis; migration; septin7; forchlorfenuron (FCF)},
	year = {2023},
	eissn = {2073-4409},
	orcid-numbers = {Szentesi, Péter/0000-0003-2621-2282; Bana, Ágnes Viktória/0009-0001-6940-1692}
}

@article{MTMT:33153168,
	title = {OGG1 Inhibition Reduces Acinar Cell Injury in a Mouse Model of Acute Pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/33153168},
	author = {Hajnády, Zoltán and Nagy-Pénzes, Máté and Demény, Máté Ágoston and Kovács, Katalin and El-Hamoly, Tarek and Maléth, József and Hegyi, Péter and Polgár, Zsuzsanna and Hegedűs, Csaba and Virág, László},
	doi = {10.3390/biomedicines10102543},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {10},
	unique-id = {33153168},
	abstract = {Acute pancreatitis (AP) is a potentially life-threatening gastrointestinal disease with a complex pathology including oxidative stress. Oxidative stress triggers oxidative DNA lesions such as formation of 7,8-dihydro-8-oxo-2′-oxoguanine (8-oxoG) and also causes DNA strand breaks. DNA breaks can activate the nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP1) which contributes to AP pathology. 8-oxoG is recognized by 8-oxoG glycosylase 1 (OGG1) resulting in the removal of 8-oxoG from DNA as an initial step of base excision repair. Since OGG1 also possesses a DNA nicking activity, OGG1 activation may also trigger PARP1 activation. In the present study we investigated the role played by OGG1 in AP. We found that the OGG1 inhibitor compound TH5487 reduced edema formation, inflammatory cell migration and necrosis in a cerulein-induced AP model in mice. Moreover, TH5487 caused 8-oxoG accumulation and reduced tissue poly(ADP-ribose) levels. Consistent with the indirect PARP inhibitory effect, TH5487 shifted necrotic cell death (LDH release and Sytox green uptake) towards apoptosis (caspase activity) in isolated pancreatic acinar cells. In the in vivo AP model, TH5487 treatment suppressed the expression of various cytokine and chemokine mRNAs such as those of TNF, IL-1β, IL1ra, IL6, IL16, IL23, CSF, CCL2, CCL4, CCL12, IL10 and TREM as measured with a cytokine array and verified by RT-qPCR. As a potential mechanism underlying the transcriptional inhibitory effect of the OGG1 inhibitor we showed that while 8-oxoG accumulation in the DNA facilitates NF-κB binding to its consensus sequence, when OGG1 is inhibited, target site occupancy of NF-κB is impaired. In summary, OGG1 inhibition provides protection from tissue injury in AP and these effects are likely due to interference with the PARP1 and NF-κB activation pathways.},
	year = {2022},
	eissn = {2227-9059},
	orcid-numbers = {Demény, Máté Ágoston/0000-0003-4623-4091; Maléth, József/0000-0001-5768-3090; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:32886684,
	title = {Tricetin Reduces Inflammation and Acinar Cell Injury in Cerulein-Induced Acute Pancreatitis: The Role of Oxidative Stress-Induced DNA Damage Signaling},
	url = {https://m2.mtmt.hu/api/publication/32886684},
	author = {Nagy-Pénzes, Máté and Hajnády, Zoltán and Regdon, Zsolt and Demény, Máté Ágoston and Kovács, Katalin and El-Hamoly, Tarek and Maléth, József and Hegyi, Péter and Hegedűs, Csaba and Virág, László},
	doi = {10.3390/biomedicines10061371},
	journal-iso = {BIOMEDICINES},
	journal = {BIOMEDICINES},
	volume = {10},
	unique-id = {32886684},
	year = {2022},
	eissn = {2227-9059},
	orcid-numbers = {Maléth, József/0000-0001-5768-3090; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:32628668,
	title = {The multitargeted receptor tyrosine kinase inhibitor sunitinib induces resistance of HER2 positive breast cancer cells to trastuzumab-mediated ADCC},
	url = {https://m2.mtmt.hu/api/publication/32628668},
	author = {Guti, Eliza and Regdon, Zsolt and Sturniolo, Isotta and Kiss, Alexandra and Kovács, Katalin and Demény, Máté Ágoston and Szöőr, Árpád and Vereb, György and Szöllősi, János and Hegedűs, Csaba and Polgár, Zsuzsanna and Virág, László},
	doi = {10.1007/s00262-022-03146-z},
	journal-iso = {CANCER IMMUNOL IMMUN},
	journal = {CANCER IMMUNOLOGY IMMUNOTHERAPY},
	volume = {71},
	unique-id = {32628668},
	issn = {1432-0851},
	abstract = {Despite recent advances in the development of novel personalized therapies, breast cancer continues to challenge physicians with resistance to various advanced therapies. The anticancer action of the anti-HER2 antibody, trastuzumab, involves antibody-dependent cell-mediated cytotoxicity (ADCC) by natural killer (NK) cells. Here, we report a repurposing screen of 774 clinically used compounds on NK-cell + trastuzumab-induced killing of JIMT-1 breast cancer cells. Using a calcein-based high-content screening (HCS) assay for the image-based quantitation of ADCC that we have developed and optimized for this purpose, we have found that the multitargeted tyrosine kinase inhibitor sunitinib inhibits ADCC in this model. The cytoprotective effect of sunitinib was also confirmed with two other assays (lactate dehydrogenase release, and electric cell substrate impedance sensing, ECIS). The drug suppressed NK cell activation as indicated by reduced granzyme B deposition on to the target cells and inhibition of interferon-γ production by the NK cells. Moreover, sunitinib induced downregulation of HER2 on the target cells' surface, changed the morphology and increased adherence of the target cells. Moreover, sunitinib also triggered the autophagy pathway (speckled LC3b) as an additional potential underlying mechanism of the cytoprotective effect of the drug. Sunitinib-induced ADCC resistance has been confirmed in a 3D tumor model revealing the prevention of apoptotic cell death (Annexin V staining) in JIMT-1 spheroids co-incubated with NK cells and trastuzumab. In summary, our HCS assay may be suitable for the facile identification of ADCC boosting compounds. Our data urge caution concerning potential combinations of ADCC-based immunotherapies and sunitinib.},
	keywords = {breast cancer; natural killer cell; trastuzumab; sunitinib; antibody-dependent cell mediated cytotoxicity (ADCC); Herceptin},
	year = {2022},
	eissn = {0340-7004},
	pages = {2151-2168}
}

@article{MTMT:32499240,
	title = {The multi-targeted receptor tyrosine kinase inhibitor sunitinib inhibits natural killer cell-mediated antibody-dependent cellular cytotoxicity against JIMT-1 breast carcinoma cells},
	url = {https://m2.mtmt.hu/api/publication/32499240},
	author = {Guti, Eliza and Hegedűs, Csaba and Regdon, Zsolt and Polgár, Zsuzsanna and Virág, László},
	journal-iso = {FEBS OPEN BIO},
	journal = {FEBS OPEN BIO},
	volume = {11},
	unique-id = {32499240},
	issn = {2211-5463},
	year = {2021},
	eissn = {2211-5463},
	pages = {405-406}
}