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. 2020 Aug 14;11:556. doi: 10.3389/fendo.2020.00556

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Copyright © 2020 Ku and Cheng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ATF3 plays a critical role in colon cancer. ATF3 overexpression could inhibit the migration and invasion of the HCT116 cells and decrease the size of mouse tumor xenografts. ATF3 promotes death receptor 5 (DR5) induction and apoptotic cell death upon zerumbone (a bioactive sesquiterpene) or celecoxib (a selective inhibitor of cyclooxygenase 2) treatment in human p53-deficient colorectal cancer cells. ATF3 is upregulated by treatment with cyclooxygenase (Cox) inhibitor (sulindac sulfide) or Cox-1 specific inhibitor SC-560 or Cox-2 specific inhibitor SC-58125, suggesting that ATF3 may be involved in sulindac sulfide/SC-560/SC-58125-induced apoptosis and anti-tumorigenic effect in human colon cancer cells. Naringenin (NAR) upregulates ATF3 expression in colon cancer cells. Furthermore, ATF3 overexpression enhances NAR-modulated cleavage of PARP. Trans-10, cis-12-conjugated linoleic acid (CLA) could increase ATF3 expression. In addition, ATF3 modulates trans-10, cis-12-CLA-stimulated non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) expression and apoptosis in colon cancer cells. These findings suggest that ATF3 acts as a tumor suppressor for colon cancer. However, siRNA-mediated knockdown of ATF3 attenuates motility and invasion of the colon cancer cell. These observations suggest that ATF3 plays a dual role in colon cancer.