Scinovex
article Open AccessTop 1% cited

YTHDF1 Regulates Tumorigenicity and Cancer Stem Cell-Like Activity in Human Colorectal Carcinoma

Frontiers in Oncology · 2019 · Vol. 9 · pp. 332–332
Yang BaiChunxing YangRunliu WuLihua HuangShenlei SongWanwan LiPeichen YanChangwei LinDaojiang LiYi Zhang

Abstract

YTH N6-methyladenosine (m6A) RNA binding protein 1 (YTHDF1) is a core factor in RNA methylation modification. Recent studies have shown that m6A is closely related to multiple tumors, thus YTHDF1 may also play a role in tumorigenesis. This study, aimed to explore the role of YTHDF1 in the colorectal cancer (CRC). In this study, we identified YTHDF1 as being highly expressed at the mRNA and protein levels in TCGA, GEO CRC and primary CRC. Furthermore, the YTHDF1 gene copy number was positively correlated with YTHDF1 mRNA expression in CRC. Knocking down the expression of YTHDF1 significantly inhibited the CRC cell's tumorigenicity <i>in vitro</i> and murine xenograft tumor growth <i>in vivo</i>. Furthermore, silencing of YTHDF1 inhibited the colonosphere formation ability <i>in vitro</i>. Mechanistically, we found that silencing YTHDF1 significantly inhibited Wnt/β-catenin pathway activity in CRC cells. Together, YTHDF1 is overexpressed in CRC and plays a vital oncogenic role in CRC, and this novel finding may provide a potential therapeutic target for CRC.

RNA modifications and cancerCancer-related gene regulationEpigenetics and DNA MethylationGene silencingCancer researchWnt signaling pathwayColorectal cancerCarcinogenesisBiologyGene knockdownCateninMethylationCancer
Citations
292
FWCI
18.59
field-weighted impact
References
49
Percentile
100%
vs. same field & year
Citations per year
References
Wnt/β-Catenin Signaling and Disease
Cell · 2012 · 5,472 citations
Colorectal cancer statistics, 2014
CA A Cancer Journal for Clinicians · 2014 · 2,565 citations
Cancer statistics in China, 2015
CA A Cancer Journal for Clinicians · 2016 · 17,930 citations
Citation Network

How this paper connects to the literature. Drag to explore, click any node to open that paper.