MYC and breast carcinoma: To explore the mechanism through which Orp degrades β-catenin, TNF-α was used to construct an inflammatory cell model in MCF-7 cells, and the proteasome inhibitor MG132 was used to treat breast cancer cells under stimulation by TNF-α and Orp. Under the effect of TNF-α, MG132 addition activated the β-catenin/c-Myc/cyclin-D1 signaling axis in MCF7 cells (Figure S3A, fourth row vs first row), whereas Orp treatment inhibited it.