FEM1B enhances TRAIL‐induced apoptosis in T lymphocytes and monocytes

FEM1B is recognized for its significant pro‐apoptotic function in colorectal cancer; however, its influence and mechanisms regarding apoptosis in immune cells remain inadequately elucidated. In this study, we demonstrated that FEM1B enhances TRAIL‐induced apoptosis in Molt‐4, Jurkat, THP‐1, and U937 cell lines. Notably, the knockdown of FEM1B in transfected cells resulted in a reversal of the observed increase in cell apoptosis. Our findings indicate that FEM1B activates caspase‐3 and caspase‐8, but not caspase‐9, in response to TRAIL stimulation, suggesting its involvement in the extrinsic caspase‐dependent apoptotic pathway. Furthermore, we found that FEM1B interacted with TRAF2 and downregulates its expression in Molt‐4 and Jurkat cells, thereby diminishing TRAF2's inhibitory effect on caspase‐8. In THP‐1 and U937 cells, FEM1B was found to upregulate TRAIL‐R2, thereby promoting TRAIL‐induced apoptosis. Knockout studies in murine models further corroborated that FEM1B facilitates TRAIL‐induced apoptosis. These results demonstrate that FEM1B enhances TRAIL‐induced apoptosis in T lymphocytes and monocytes through a caspase‐dependent mechanism involving TRAF2 or TRAIL receptors.

Abstract licence: CC BY

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