2. Ερευνητικές δημοσιεύσεις | Research publications

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Η συλλογή αυτή συγκεντρώνει τις δημοσιεύσεις του διδακτικού και ερευνητικού προσωπικού του Πανεπιστημίου Πατρών σε επιστημονικά περιοδικά ή σε επιστημονικές εκδηλώσεις (συνέδρια, ημερίδες, κλπ.).

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Browsing 2. Ερευνητικές δημοσιεύσεις | Research publications by Author "Apostolopoulou, Hara"

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    Myeloid-derived interleukin-1β drives oncogenic KRAS-NF-κΒ addiction in malignant pleural effusion
    Marazioti, Antonia; Lilis, Ioannis; Vreka, Malamati; Apostolopoulou, Hara; Kalogeropoulou, Argyro; Giopanou, Ioanna; Giotopoulou, Georgia; Krontira, Anthi; Iliopoulou, Marianthi; Kanellakis, Nikolaos; Agalioti, Theodora; Giannou, Anastasios; Jones-Paris, Celestial; Iwakura, Yoichiro; Kardamakis, Dimitrios; Blackwell, Timothy; Taraviras, Stavros; Spella, Magda; Stathopoulos, Georgios; Μαραζιώτη, Αντωνία; Λιλής, Ιωάννης; Βρεκά, Μαλαματή; Αποστολοπούλου, Χαρά; Καλογεροπούλου, Αργυρώ; Γιοπάνου, Ιωάννα; Γιωτοπούλου, Γεωργία; Κροντηρά, Ανθή; Ηλιοπούλου, Μαριάνθη; Κανελλάκης, Νικόλαος; Αγαλιώτη, Θεοδώρα; Γιάννου, Αναστάσιος; Καρδαμάκης, Δημήτριος; Ταραβήρας, Σταύρος; Σπέλλα, Μάγδα; Σταθόπουλος, Γεώργιος
    Τμήμα Ιατρικής (Δημοσ. Π.Π. σε περιοδικά)
    Malignant pleural effusion (MPE) is a frequent metastatic manifestation of human cancers. While we previously identified KRAS mutations as molecular culprits of MPE formation, the underlying mechanism remained unknown. Here, we determine that non-canonical IKKα-RelB pathway activation of KRAS-mutant tumor cells mediates MPE development and this is fueled by host-provided interleukin IL-1β. Indeed, IKKα is required for the MPE-competence of KRAS-mutant tumor cells by activating non-canonical NF-κB signaling. IL-1β fuels addiction of mutant KRAS to IKKα resulting in increased CXCL1 secretion that fosters MPE-associated inflammation. Importantly, IL-1β-mediated NF-κB induction in KRAS-mutant tumor cells, as well as their resulting MPE-competence, can only be blocked by co-inhibition of both KRAS and IKKα, a strategy that overcomes drug resistance to individual treatments. Hence we show that mutant KRAS facilitates IKKα-mediated responsiveness of tumor cells to host IL-1β, thereby establishing a host-to-tumor signaling circuit that culminates in inflammatory MPE development and drug resistance.