Consistent with findings that AP-1 promoted invasiveness of triple-negative breast cancer [38] and squamous cell carcinoma [39], knockdown of JUN/FOSL2 inhibited invasion of AR-expressing ESCC cells without influencing cell growth ability, suggesting that the JUN/FOSL2/AR transcriptional axis may especially exert its function in ESCC metastasis. This evidence concerns the gene JUN and triple-negative breast carcinoma.