lncRNA B4GALT1‐AS1 promotes colon cancer cell stemness and migration by recruiting YAP to the nucleus and enhancing YAP transcriptional activity

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Abstract
Here, an RNA‐sequencing assay revealed long noncoding RNAs (lncRNAs) with an ectopic expression between colon cancer (CC) and normal colon epithelial cells, in which lncRNA B4GALT1‐AS1 exhibited the highest change. A 3‐(4,5‐dimethythiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay indicated that B4GALT1‐AS1 knockdown had no effect on CC cell viability, however, cell clone formation analysis showed that B4GALT1‐AS1 knockdown attenuated the capacity of cell clone formation. Additionally, gene set enrichment analysis of this data set revealed that positive enrichment of stem cell‐differentiated signatures and negative embryonic stem cell function and adult tissue stem module were observed in CC cells with B4GALT1‐AS1 knockdown. Furthermore, B4GALT1‐AS1 knockdown suppressed the stemness‐marker expression, the ability of cell spheroid formation, and ALDH1 activity in CC cells. Mechanistically, RNA‐sequencing data found that the Hippo pathway in cancer was shown on pathways mostly upregulated by B4GALT1‐AS1 knockdown, and B4GALT1‐AS1 directly bound to the yes‐associated protein (YAP), a downstream executor of the Hippo pathway, and B4GALT1‐AS1 knockdown promoted the nuclear cytoplasm translocation of YAP and decreased YAP transcriptional activity. Notably, YAP overexpression attenuated the inhibitory effects mediated by B4GALT1‐AS1 knockdown. Our results identify the direct binding of lncRNA B4GALT1‐AS1 to YAP, which is responsible for CC cell stemness.

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