Oncogene Lin28B increases chemosensitivity of colon cancer cells in a let-7-independent manner.

Lin-28 homolog B (Lin28B) is a RNA binding protein conserved between Caenorhabditis elegans and humans, and it has important roles in regulating development. The overexpression of Lin28B has been observed in various human malignant tumors and the upregulation of Lin28B predicts tumor progression and/or poor prognosis. The majority of studies suggested that Lin28B is an oncogene that promotes the proliferation and metastasis of cancer cells. However, few studies have focused on the function of Lin28B in chemotherapy. In the present study, the role of Lin28B in the chemosensitivity of colon cancer cells to 5-fluorouracil (5-FU) was detected by establishing a Lin28B over-expressing HCT116 (EGFP-Lin28B-HCT116) cell line. In accordance with the immunohistochemistry results, Lin28B-GFP expression was predominantly distributed in the cytoplasm, and the overexpression of Lin28B was confirmed using quantitative polymerase chain reaction and western blot analysis. The control EGFP-HCT116 and Lin28B over-expressing EGFP-Lin28B-HCT116 cells were then exposed to various concentrations of 5-FU for 48 h. A luminescence-based cell viability assay was used to detect the effect of Lin28B on the chemotherapeutic sensitivity of colon cancer cells. It was demonstrated that overexpression of Lin28B improved the chemotherapeutic sensitivity of colon cancer cells to 5-FU. Additional investigation revealed that Lin28B enhanced the chemosensitivity of colon cancer cells by promoting cell apoptosis induced by 5-FU; however, this effect was independent of Lin28B inhibiting the biogenesis of let-7, the well-known target of Lin28B. The mechanism of this effect of Lin28B on the chemosensitivity of cells requires additional investigation. The present study suggested that Lin28B may act as a biomarker for predicting chemotherapy sensitivity in patients with colon cancer.