BMPR1A promotes the proliferation of colorectal cancer cells through the activation of Smad1

Abstract Objectives Colorectal cancer (CRC) is the second leading cause of cancer-related deaths globally. Although bone morphogenetic protein receptor type 1A (BMPR1A) is recognized for its important role in tumor development, the precise mechanism by which it acts in CRC necessitates additional research. Our study aimed to investigate the role and mechanism of BMPR1A in CRC. Methods Using the Gene Expression Profiling Interactive Analysis (GEPIA) database, we analyzed BMPR1A expression in CRC. We investigated the effects of BMPR1A on cell proliferation, migration, invasion, and cell cycle, and the regulation of Smad1. In addition, a mouse xenograft model was established. Results The GEPIA database revealed that elevated expression levels of BMPR1A correlate with higher mortality rates and shorter survival duration in patients with CRC. Following the knockdown of BMPR1A, SW620 and HCT116 cells exhibited a decrease in the rate of value addition, arrest of the cell cycle, and a heightened rate of apoptosis, alongside a reduction in migratory and invasive capabilities. Tumor growth was inhibited after the injection of cells with si-BMPR1A in CRC mouse models. Further investigation demonstrated that SMAD family member 1 (Smad1) is activated by BMPR1A. Inhibition of the BMPR1A/Smad1 pathway was found to block p38 pathway activation and mitigate CRC progression. Conclusions BMPR1A could have a crucial function in the development of CRC through the activation of Smad1, and governs related downstream processes. Targeting BMPR1A provides a foundation for novel therapeutic strategies in CRC.