LIN28B promotes the progression of colon cancer by increasing B-cell lymphoma 2 expression.

RNA-binding protein LIN28B is frequently overexpressed in human colon cancer and is associated with the tumor progression and poor prognosis. The potential molecular mechanisms underlying the role of LIN28B in colon cancer remain unclear. The present study aimed to explore the role of B-cell lymphoma 2 (BCL-2) in promoting colon cancer development associated with LIN28B. The expression pattern of LIN28B in colon cancer tissues and cell lines was detected by RT-PCR, Western blotting analysis, and immunohistochemical staining. A log rank test was carried out to compare the survival times of patients with high/low levels of LIN28B. The effects of LIN28B on cell clonal formation, growth, and apoptosis were detected by clone formation, MTT and flow cytometry assays, respectively. BCL-2 expression and protein stability after LIN28B up-regulation were assessed by Western blotting. The effects of LIN28B and BCL-2 on tumorigenesis were evaluated by an in vivo xenograft assay. The results showed that LIN28B was highly expressed in colon cancer tissues and cell lines, which could promote cell clonal formation and growth and inhibit cell apoptosis. Up-regulation of LIN28B increased BCL-2 expression, enhanced its stability, and reduced its ubiquitination. Overexpression of LIN28B promoted cell tumorigenesis, whereas this effect was repressed by knockdown of BCL-2. This study suggests that overexpression of LIN28B promotes colon cancer development by increasing BCL-2 expression, potentially opening up new avenues for therapeutic approaches to colon cancer treatment.