Arsenic and the compounds thereof can be carcinogens or therapeutic agents for different cancer types. However, for breast cancer (BC), studies have yielded conflicted results on the role of arsenic. A previous study by the present authors indicated a potential relationship between circDHX34 and sodium arsenite-treated BC cells. As such, the expression, function, and potential mechanism of circDHX34 in sodium arsenite-treated MDA-MB-231 cells were further detected. In the present study, findings were made that sodium arsenite upregulated circDHX34 expression in MDA-MB-231 cells in a dose-dependent manner, and knockdown of circDHX34 could promote cell proliferation and inhibit apoptosis. Further investigations revealed that knockdown of circDHX34 upregulated the expression levels of antiapoptotic genes BCL2 and BCL2L1 and downregulated the expression levels of proapoptotic genes CASP8 and CASP9. To conclude, by regulating apoptotic genes, sodium arsenite-mediated upregulation of circDHX34 promotes apoptosis in hormone-independent breast cancer cells.