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The discovery of a potent gene regulating tumorigenesis and drug resistance is of high clinical importance.  STIL  is an oncogene; however, its molecular associations and role in colorectal oncogenesis are unknown. In this study, we have explored the role of  STIL  gene in tumorigenesis and studied its molecular targets in colorectal cancer (CRC).  STIL  silencing reduced proliferation and tumor growth in CRC. Further, STIL was found to regulate stemness markers  CD133  and  CD44  and drug resistant markers  thymidylate synthase ,  ABCB1 , and  ABCG2  both in  in-vitro  and  in-vivo  CRC models. In addition, high expression of  STIL  mRNA was found to be associated with reduced disease-free survival in CRC cases. Interestingly, we observed that  STIL -mediated regulation of stemness and drug resistant genes is not exclusively governed by Sonic hedgehog (Shh) signaling. Remarkably, we found  STIL  regulate β-catenin levels through p-AKT, independent of Shh pathway. This partially answers Shh independent regulatory mechanism of cancer stem cell (CSC) markers by  STIL . Our study suggests an instrumental role of  STIL  in molecular manifestation of CRC and progression.

STIL Endows Oncogenic and Stem-Like Attributes to Colorectal Cancer Plausibly by Shh and Wnt Signaling