NAT10 promotes gastric cancer metastasis via N4-acetylated COL5A1

2021-05-03 阅读

Yigan ZhangYuanxue JingYinxue WangJianming TangXiaoran ZhuWei-Lin JinYiqing WangWenzhen YuanXiangkai Li, and Xun LiYigan ZhangYuanxue JingYinxue WangJianming TangXiaoran ZhuWei-Lin JinYiqing WangWenzhen YuanXiangkai Li, and Xun Li

Signal Transduct Target Ther

Dear Editor,

Gastric cancer (GC) is among the most prevalent gastrointestinal malignancies. The occurrence of local deep infiltration or distant metastasis in GC is commonly associated with weak treatment and poor prognosis.1 Although, N4-Acetylcytidine (ac4C) represents one of the extensive chemical modifications in mRNAs that plays a pivotal role in modulating mRNA stability and the mRNA translation process (Fig. 1b). However, the role of mRNA ac4C modification in disease remains unclear.2 As the only known ac4C “writer” protein, NAT10 is thought to have critical effects in tumor metastasis and tumor cell epithelial-to-mesenchymal transition (EMT). Here, we report a novel mechanism of NAT10-mediated mRNA ac4C modification regulating gastric cancer metastasis and EMT.

URL:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8093205/