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ABSTRACT
Chemoresistance in hepatocellular carcinoma (HCC) has been found to be influenced by exosomal transport of circRNAs. However, the role of circZFR in HCC chemoresistance still remains unclear. In the present study, circZFR was highly expressed in cisplatin (DDP)-resistant HCC cell lines and could regulate DDP resistance of the HCC cells. Also, circZFR was highly expressed in cancer-associated fibroblast (CAFs) and the exosome of CAFs. In addition, supplementation of CAFs in culture medium could promote DDP resistance of HCC cells. In vivo tumor xenograft experiments showed that knockdown of circZFR inhibited tumor growth and weakened DDP resistance, while CAFs-derived exosomes incubation increased the expression of circZFR, inhibited the STAT3/NF-κB pathway, promoted tumor growth, and enhanced DDP resistance. In general, CAFs-derived exosomes deliver circZFR to HCC cells, inhibit the STAT3/NF-κB pathway, and promote HCC development and chemoresistance. The results provided a new sight for the prevention and treatment of chemoresistance in HCC.
Graphical abstract
Highlights
CircZFR was highly expressed in DDP-resistant HCC cells and promoted DDP resistance.
CAFs-derived exosomes promote DDP resistance of HCC through circZFR in vitro and in vivo.
CAFs-derived exosomes deliver circZFR to HCC cells and inhibit the STAT3/NF-κB pathway.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The datasets analyzed during the current study are available from the corresponding author on reasonable request.
Supplementary material
Supplemental data for this article can be accessed here
