Abstract
LIN28B is involved in “stemness” and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.
Highlights
LIN28 was initially identified in C. elegans and was shown to be responsible for the timing of development [1]
Because Let-7 functions as a potential growth suppressor in human colon cancer cells [15], we examined LIN28B expression in colon cancer tissues to determine the balance between LIN28B and let-7 expression
Our results reveal that LIN28B expression is closely related to overall patient survival and recurrence of colon cancer
Summary
LIN28 was initially identified in C. elegans and was shown to be responsible for the timing of development [1]. LIN28B, as a homologue of LIN28, was first cloned from and shown to be overexpressed in human hepatocellular carcinoma cells and clinical samples in 2006 [2]. LIN28B is a developmentally regulated RNA-binding protein that promotes tumourigenesis by blocking the post-transcriptional processing of the tumour-suppressive pri-/pre-let-7 microRNA [3,4]. The ability of LIN28B to regulate let-7, a bona fide tumoursuppressor, is consistent with its developmental role in regulating cell proliferation and differentiation. Besides let-7, LIN28B may bind the mRNA of intestinal stem cell markers, such as LGR5 and PROM1 [6]. LIN28B promotes transformation primarily by suppressing let-7. Competition between LIN28B and let-7 may be critical for normal cell biology and may accelerate tumour development once this balance is perturbed
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