Given that c-Jun and p-c-Jun acted as a transcription factor in colorectal cancer [34], breast cancer [35], and acute lymphoblastic leukemia [36], and the JASPAR database indicated the presence of c-Jun-binding sites in the promoter region of SPARC, we hypothesized that LCN2 inhibits the JNK/c-Jun signaling pathway and weakens the transcriptional activity of c-Jun and p-c-Jun to SPARC, ultimately leading to SPARC downregulation. This evidence concerns the gene JUN and breast carcinoma.