The CXCR4 antagonist R54 targets epithelial-mesenchymal transition (EMT) in human ovarian cancer cells

The axis CXCL12-CXCR4 is highly expressed in ovarian cancer where contributes to disease progression. Aim of the work was to evaluate the effect of the newly developed CXCR4 antagonist R54 on human ovarian cancer cells aggressiveness. CXCL12-CXCR4 axis was evaluated in human ovarian cancer cells thr...

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Veröffentlicht in:	PloS one 2024-12, Vol.19 (12), p.e0314735
Hauptverfasser:	Russo, Daniela, Spina, Anna, Portella, Luigi, Bello, Anna Maria, Galdiero, Francesca, Trotta, Anna Maria, Ieranò, Caterina, Rea, Giuseppina, Cecere, Sabrina Chiara, Coppola, Elisabetta, Di Maro, Salvatore, Pignata, Sandro, Califano, Daniela, Scala, Stefania
Format:	Artikel
Sprache:	eng
Schlagworte:	Antibodies Biology and Life Sciences Cadherins - metabolism Cancer Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Chemokine CXCL12 - metabolism Chemoresistance CXCL12 protein CXCR4 protein E-cadherin Epithelial-Mesenchymal Transition - drug effects Female Flow cytometry Humans Immunoblotting Immunofluorescence Ligands Medicine and Health Sciences Molecular weight N-Cadherin Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology Penicillin Proteins Receptors, CXCR4 - antagonists & inhibitors Receptors, CXCR4 - metabolism Research and Analysis Methods Signal Transduction - drug effects Vimentin Vimentin - metabolism
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Zusammenfassung:	The axis CXCL12-CXCR4 is highly expressed in ovarian cancer where contributes to disease progression. Aim of the work was to evaluate the effect of the newly developed CXCR4 antagonist R54 on human ovarian cancer cells aggressiveness. CXCL12-CXCR4 axis was evaluated in human ovarian cancer cells through proliferation, migration and signaling CXCL12-dependents. Epithelial to mesenchymal transition (EMT) was analyzed through E-CADHERIN, N-CADHERIN, VIMENTIN, SNAIL1 and ΒETA-CATENIN by qRT-PCR, immunofluorescence and immunoblotting. R54 inhibited ovarian cancer cells proliferation and migration CXCL12-induced. Moreover, R54 inhibited CXCL12 dependent pERK1/2 and pAKT and reversed the CXCL12 induced EMT in ovarian cancer cells. Targeting CXCR4 with the new antagonist R54 consistently reverted the mesenchymal transition in human ovarian cancer cells reducing migratory and chemoresistance features.
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0314735