OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer.

Abstract

OCT4B1, a splice variant of OCT4, is a key regulator in maintaining the properties of pluripotency and self-renewal in embryonic stem (ES) cells. Recent results have shown that OCT4B1 is involved in tumorigenesis. However, the contribution of OCT4B1 in the tumorigenesis and drug resistance of colon cancer remains to be determined. The aim of the present study was to determine whether OCT4B1, which maintains the stemness of ES cells, promoted cell growth by facilitating transition of the cell cycle and reduced apoptosis in colon cancer and drug‑resistant cells using flow cytometry and western blotting. The results showed that, OCT4B1 promoted the growth of colon cancer and drug‑resistant cancer cells by maintaining the activity of ES cells and by facilitating the transition of the cell cycle and reducing apoptosis. Additionally, OCT4B1 was able to reduce sensitivity to oxaliplatin by altering the expression of two important mediators in drug resistance, P-gp and ABCG2 [ATP-binding cassette, sub‑family G (WHITE), member 2]. Furthermore, OCT4B1 enhanced the ability of migration and invasion through alteration of the epithelial-to-mesenchymal transition (EMT) in colon cancer. In conclusion, to the best of our knowledge, the results demonstrated for the first time that OCT4B1 functions as an oncogene in colon cancer and provides the development of novel therapeutic strategies to treat colon cancer, particularly drug resistance.