【摘 要】
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Cisplatin resistance is a major challenge for bladder cancer(BC).Evidence indicates that exo-some derived from cancer-associated fibroblasts(CAF-Exo)can promote
【机 构】
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Department of Urology,The First Affiliated Hospital of Anhui Medical University,Hefei 230022,China;I
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Cisplatin resistance is a major challenge for bladder cancer(BC).Evidence indicates that exo-some derived from cancer-associated fibroblasts(CAF-Exo)can promote chemotherapy resistance in various human tumors by delivering bioactive molecules.We have previously demonstrated that CAF-derived exosomal LINC00355 promotes BC cell proliferation and invasion.However,the underlying mechanisms are still unclear.In this study,we aimed to investigate the role and mech-anisms of CAF-derived exosomal LINC00355 in BC cell resistance to cisplatin.Exosomes were isolated from normal fibroblasts(NFs)and BC tumor-derived CAFs,namely,NF-Exo and CAF-Exo.CAFs were transfected with si-Ctrl or si-LINC00355 and then different exosomes were isolated,namely,CAFsi-Ctrl-Exo and CAFsi-LINC00355-Exo.The human BC cell lines(T24 and 5367)were incu-bated with NF-Exo,CAF-Exo,CAFsi-Ctrl-Exo,and CAFsi-LINC00355-Exo in the presence of cisplatin.MTT proliferation assay and flow cytometric analysis showed that CAF-Exo promoted BC cell resis-tance to cisplatin and upregulated ABCB1 expression in BC cells by transferring LINC00355 to BC cells.Luciferase activity assay confirmed the interaction between miR-34b-5p and LINC00355 or ABCB1.qRT-PCR and western blot analysis further showed that LINC00355 sponged miR-34b-5p to upregulate ABCB1 expression.However,the promoting effects of CAF-Exo on BC cell resistance to cisplatin were abolished by miR-34b-5p overexpression and ABCB1 silencing.In conclusion,exosomal LINC00355 derived from CAFs promotes BC cell resistance to cisplatin by regulating the miR-34b-5p/ABCB1 axis.
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