Molecular biological analysis of radiation induced epithelial-mesenchymal transition on cancer stem cell of rectal cancer

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We hypothesized that residual cancer cells after chemoradiotherapy (CRT) for rectal cancer have the treatment (CRT)-resistant property and contain putative CSCs, compared with pre-CRT cancer specimens. Furthermore, residual cancer cells which survived CRT may acquire metastatic potential induced by EMT. The expression of CD133, leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5), glucose transporter 1 (GLUT1), and hypoxia inducible factor-1α (HIF-1α) on residual cancer cells after CRT was associated with cancer recurrence and patient prognosis. The expression of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) on residual cancer cells after CRT was also associated with cancer recurrence. The expression of CXCR4 and its ligand CXCL12, fibroblast activation protein-α (FAP-α), and stromal cell-derived factor-1 (SDF-1) on the cancer stroma after CRT was also associated with cancer recurrence and patient prognosis. In vitro study, radiation induced EMT in colorectal cancer cells, resulting in the acquisition of invasive and metastatic properties. Neurotrophic receptor tropomyosin related kinase (TrkB) also induced EMT in colorectal cancer cells. TrkB was inversely correlated with E-cadherin, and associated with poor prognosis of colorectal cancer patients. CD133 was increased in a radiation dose-dependent manner, despite of the decreased number of clonogenic radiation-surviving cells.