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- W3158668786 abstract "Abstract Background The tumor microenvironment plays an important role in promoting chemoresistance in solid cancers. This study aimed to evaluate the underlying molecular mechanisms in the tumor microenvironment potentially involved in chemoresistance in lung adenocarcinoma patients. Methods A multiplex assay was used to determine the transcription factor levels in chemoresistant lung adenocarcinoma cells. The role of chemokine (C-C motif) ligand 2 (CCL2) in chemoresistance of lung adenocarcinoma was evaluated both in vitro and in vivo . A ChIP assay was performed to determine the molecular mechanism by which c-Fos regulates “CCL2”. Results CCL2 expression was significantly higher in chemoresistant than in chemosensitive lung adenocarcinoma cells and was closely associated with poor survival in lung adenocarcinoma patients. CCL2 enhanced the resistance of lung adenocarcinoma cells to cisplatin in vitro . Chemoresistant lung adenocarcinoma cell-derived CCL2 promoted monocyte recruitment to the tumor site and monocyte polarization into M2 macrophages, which further mediated the chemoresistance of lung adenocarcinoma. The involvement of c-Fos in CCL2 expression in lung adenocarcinoma cells might promote chemoresistance. Blockade of CCL2 suppressed tumor growth and restored cisplatin sensitivity in lung adenocarcinoma. Conclusions The c-Fos–CCL2 axis might provide a promising target for the treatment of lung adenocarcinoma." @default.
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- W3158668786 date "2021-05-05" @default.
- W3158668786 modified "2023-09-27" @default.
- W3158668786 title "Tumor cell-derived CCL2 promotes chemoresistance via c-Fos in lung adenocarcinoma" @default.
- W3158668786 doi "https://doi.org/10.21203/rs.3.rs-450308/v1" @default.
- W3158668786 hasPublicationYear "2021" @default.
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