STIL silencing begets EMT-like molecular alterations in colorectal cancer

Metastasis remains a major challenge in colorectal cancer (CRC) treatment. STIL is an oncogene, dysregulated in multiple cancers and has been known to regulate cancer stem cell maintenance through Sonic Hedgehog and Wnt signaling pathways in CRC. Although STIL has been implicated in invasion, migration, and metastasis in several malignancies, its role in CRC metastatic progression remains unclear. In the present study, we investigated the effect of STIL silencing on epithelial-mesenchymal transition (EMT)-associated markers in CRC. STIL knockdown both in in vitro and in vivo models resulted in reduced E-cadherin expression and increased N-cadherin and Vimentin expression, indicating EMT-associated molecular alterations. Similar expression trends and correlations were further supported by GEPIA-based analyses and clinical CRC samples. These findings suggest that STIL may play a complex and context-dependent role in CRC progression and EMT regulation. Overall, the present study provides preliminary evidence linking STIL to EMT-associated pathways in CRC and highlights the need for further mechanistic and functional studies to define its role in metastasis.