FIGURE 8.

A proposed model elucidating the mechanism by which nuclear export of BATF2 promotes colorectal cancer (CRC) progression. In normal colon cells, BATF2 suppresses activator protein 1 (AP‐1) activity and its downstream oncogene expression, keeping cells from over‐proliferation. In CRC cells, the highly expressed chromosome region maintenance 1 (CRM1) interacts with BATF2 to form a complex via directly binding to its nuclear export sequence (NES) region, which translocates into the cytoplasm, leading to an ubiquitin‐mediated degradation of BATF2 and subsequent activated AP‐1‐driven cell proliferation, ultimately contributing to cancer growth.