The abstract is read at the publisher; the summary is JClub's.
XPO5 is linked to advanced prostate cancer progression by promoting ferroptosis resistance through MITF nuclear export and suppression of ACSL4 transcription.
- Why it matters: Advanced PCa needs new ways to overcome ferroptosis resistance, and the XPO5–MITF–ACSL4 regulatory mechanism was unclear.
- What they did: Single-cell and bulk RNA sequencing plus retrospective patient analyses were used to map the XPO5–MITF–ACSL4 axis, and high-throughput screening identified 2-B8 as an XPO5 molecular glue degrader.
- The result: 2-B8 covalently binds XPO5 at Cys1157, drives XPO5 ubiquitination and degradation, induces ferroptosis, suppresses tumor growth, and enhances chemosensitivity in cellular, cell-derived xenograft, and patient-derived xenograft models.
The findingWhy it mattersWhat they didThe result
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