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BACKGROUND: cells. METHODS: HCC. We then knocked down CD73 in cells, and then assessed the effect of CD73 on the apoptosis by flow cytometry. Finally, a sphere formation assay was applied to investigate the stemness of cancer cells, and xenograft tumors in nude mice were built to investigate the tumorigenicity. RESULTS: tumor cells. CONCLUSIONS: Our findings collectively suggest that CD73 is a vital HCC-chemoresistance force controlled by cross-talking between CAFs and HCC cells, thereby establishing CD73 as a potential new therapeutic target for HCC.
Peng et al. (Wed,) studied this question.