SLITRK6 in Cancer Metastasis: Emerging Evidence, Mechanisms and Therapeutic Potential

Abstract

Cancer metastasis is a complicated biological process where cells from the primary tumour site spread into other organs far from the origin and cause a secondary tumour. The cascade of metastasis includes epithelial to mesenchymal transition (EMT), in which cancerous cells lose the epithelial characters and acquire features of migration and invasion through key signalling pathways as TGF-β, Wnt/β-catenin, and Notch. After EMT, cells can intravasate into the blood or lymphatic vessels, and extravasate into remote tissues, causing secondary tumours. Current cancer therapies are often ineffective against metastatic disease, and therefore, new approaches that target metastasis specifically are needed.

SLIT and NTRK-like family member 6 (SLITRK6) promotes the migration of cancer cells by binding to ROBO receptors and controlling Rho GTPases, which are essential for cytoskeletal dynamics. Moreover, it also impacts the tumor microenvironment by regulating the interactions of immune cells and by promoting the secretion of MMPs, which facilitate tissue invasion. This review discusses the current understanding of SLITRK6's biological functions, especially in the context of cancer, and discusses the molecular pathways through which it influences metastasis. By targeting SLITRK6, it may be possible to disrupt both the migratory behavior of cancer cells and the supportive microenvironment that facilitates metastasis. Recent studies have identified SLITRK6 as a significant player in cancer metastasis. Its expression is associated with poor prognosis in several cancers. This review aims to provide a comprehensive overview of SLITRK6 in cancer metastasis and its potential as a novel therapeutic target.