BCAP31 is involved in modulating colorectal cancer cell proliferation via the Emerin/β-catenin axis

Understanding the mechanisms of colorectal cancer (CRC) progression is critical for developing innovative treatment strategies. As an endoplasmic reticulum-located protein, B cell receptor-associated protein 31 (BCAP31) has been identified to be highly expressed in multiple cancers. However, its function and molecular mechanism in CRC remain not fully understood. In the present study, BCAP31 expression and its correlation with the clinical stage were analyzed based on TCGA database. We demonstrated that loss of BCAP31 suppressed CRC cell proliferation in vitro and tumor growth in vivo. Mechanistically, we demonstrated that Emerin was an interaction partner and downstream molecule of BCAP31. Knockdown of BCAP31 promoted the nuclear envelope localization of Emerin, leading to a reduction of β-catenin accumulation in the nucleus, which resulted in downregulation of Wnt/β-catenin downstream target genes, including c-Myc, cyclin D1, Survivin, and Mcl-1. Moreover, downregulation of Emerin partially restored the BCAP31 depletion-mediated β-catenin protein level and tumor suppressive effects in CRC cells.Our data highlights the pivotal role of BCAP31 depletion in inhibiting cell proliferation in CRC cells, and mechanistically via Emerin/β-catenin signaling, which may serve as a promising target for CRC treatment. • Knockdown of BCAP31 inhibited proliferation of CRC cells in vitro and in vivo. • Knockdown of BCAP31 suppressed the Wnt/β-catenin pathway through inhibiting the nuclear accumulation of β-catenin. • Knockdown of BCAP31 exerts the tumor suppressive effects via Emerin/β-catenin pathway in CRC cells.