MO-2097 inhibits EMT and angiogenesis in colorectal cancer by targeting RAF/MEK/ERK signaling

Colorectal Cancer is a leading cause of cancer-related deaths, with metastasis being the primary contributor to its poor prognosis. Despite the development of various therapeutic strategies, metastatic colorectal Cancer prognosis still needs improvement. MO-2097, a novel therapeutic compound, was evaluated for its potential to inhibit metastasis by targeting critical processes such as Cancer cell migration and invasion. The ability of MO-2097 to inhibit Cancer cell migration was confirmed through wound healing and trans-well migration assays. Further investigation using western blot analysis revealed that MO-2097 inhibited the Raf/MEK/ERK signaling pathway by destabilizing RAF-1, a key regulator of Cancer progression and metastasis. Moreover, MO-2097 treatment led to the downregulation of mesenchymal markers N-Cadherin and Vimentin while reducing the expression of EMT-related transcription factors such as Snail, Slug, and ZEB1. In a 3D spheroid invasion model, MO-2097 significantly inhibited Cancer cell invasion by reducing their ability to penetrate the extracellular matrix. Furthermore, MO-2097 disrupted the vascular network formation in HUVECs, indicating its impact on angiogenesis, a process essential for tumor growth and metastasis. These findings demonstrate MO-2097's promise as both an anti-metastatic and anti-angiogenic agent, offering a novel therapeutic approach for treating metastatic colorectal Cancer and emphasizing its potential for future clinical applications.

3D spheroid invasion; Anti-angiogenesis; Anti-metastasis agent; Epithelial-Mesenchymal transition (EMT); RAF-1 inhibitor.