CXCR4拮抗剂R54靶向人卵巢癌细胞中的上皮-间质转化（EMT）。
The CXCR4 antagonist R54 targets epithelial-mesenchymal transition (EMT) in human ovarian cancer cells.
作者信息
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
机构信息
Microenvironment Molecular Targets, Istituto Nazionale Tumori-IRCCS-Fondazione "G. Pascale", Naples, Italy.
Uro-Gynecologic Oncology Unit, Istituto Nazionale Tumori IRCCS-Fondazione "G. Pascale", Naples, Italy.
出版信息
PLoS One. 2024 Dec 19;19(12):e0314735. doi: 10.1371/journal.pone.0314735. eCollection 2024.
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.
轴CXCL12 - CXCR4在卵巢癌中高表达，其有助于疾病进展。本研究的目的是评估新开发的CXCR4拮抗剂R54对人卵巢癌细胞侵袭性的影响。通过增殖、迁移和CXCL12依赖性信号传导来评估人卵巢癌细胞中的CXCL12 - CXCR4轴。通过qRT - PCR、免疫荧光和免疫印迹，利用E - 钙黏蛋白、N - 钙黏蛋白、波形蛋白、SNAIL1和β - 连环蛋白分析上皮 - 间充质转化（EMT）。R54抑制CXCL12诱导的卵巢癌细胞增殖和迁移。此外，R54抑制CXCL12依赖性的pERK1/2和pAKT，并逆转CXCL12诱导的卵巢癌细胞EMT。用新型拮抗剂R54靶向CXCR4可一致地逆转人卵巢癌细胞的间充质转化，降低其迁移和化疗耐药特性。
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