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001-es BibID:	BIBFORM103842
035-os BibID:	(Scopus)85129934393 (cikkazonosító)e0268217
Első szerző:	Bohusné Barta Bettina
Cím:	Survival of HT29 cancer cells is influenced by hepatocyte growth factor receptor inhibition through modulation of self-DNA-triggered TLR9-dependent autophagy response / Bettina Bohusné Barta, Ágnes Simon, Lőrinc Nagy, Titanilla Dankó, Regina Eszter Raffay, Gábor Petővári, Viktória Zsiros, Anna Sebestyén, Ferenc Sipos, Györgyi Műzes
Dátum:	2022
ISSN:	1932-6203
Megjegyzések:	HGFR activation drives the malignant progression of colorectal cancer, and its inhibition displays anti-autophagic activity. The interrelated role of HGFR inhibition and TLR9/autophagy signaling in HT29 cancer cells subjected to modified self-DNA treatments has not been clarified. We analyzed this complex interplay with cell metabolism and proliferation measurements, TLR9, HGFR and autophagy inhibitory assays and WES Simple Western blot-based autophagy flux measurements, gene expression analyses, immunocytochemistry, and transmission electron microscopy. The overexpression of MyD88 and caspase-3 was associated with enhanced HT29 cell proliferation, suggesting that incubation with self-DNAs could suppress the apoptosis-induced compensatory cell proliferation. HGFR inhibition blocked the proliferation-reducing effect of genomic and hypermethylated, but not that of fragmented DNA. Lowest cell proliferation was achieved with the concomitant use of genomic DNA, HGFR inhibitor, and chloroquine, when the proliferation stimulating effect of STAT3 overexpression could be outweighed by the inhibitory effect of LC3B, indicating the putative involvement of HGFR-mTOR-ULK1 molecular cascade in HGFR inhibitor-mediated autophagy. The most intense cell proliferation was caused by the co-administration of hypermethylated DNA, TLR9 and HGFR inhibitors, when decreased expression of both canonical and non-canonical HGFR signaling pathways and autophagy-related genes was present. The observed ultrastructural changes also support the context-dependent role of HGFR inhibition and autophagy on cell survival and proliferation. Further investigation of the influence of the studied signaling pathways and cellular processes can provide a basis for novel, individualized anti-cancer therapies.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Plos One. - 17 : 5 (2022), p. 1-25. -
További szerzők:	Simon Ágnes Nagy Lőrinc (1995-) (biológus, gyógyszer-biotechnológus) Dankó Titanilla Raffay Regina Eszter Petővári Gábor Zsiros Viktória Sebestyén Anna Sipos Ferenc (belgyógyász) Műzes Györgyi
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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