Novel Long Noncoding RNA miR205HG Functions as an Esophageal Tumor-Suppressive Hedgehog Inhibitor.
Novel Long Noncoding RNA miR205HG Functions as an Esophageal Tumor-Suppressive Hedgehog Inhibitor.
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新的非编码长链RNA miR205HG作为食道肿瘤抑制因子发挥作用。
DOI：
10.3390/cancers13071707
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发表时间：
2021-04-03
期刊：
影响因子：
5.2
通讯作者：
Meltzer SJ
中科院分区：
文献类型：
--
作者：
Song JH;Tieu AH;Cheng Y;Ma K;Akshintala VS;Simsek C;Prasath V;Shin EJ;Ngamruengphong S;Khashab MA;Abraham JM;Meltzer SJ
Barrett的食管（BE）是食管腺癌（EAC）的前体。当前研究的目的是：（1）研究MiR205HG在BE和EAC的开发中阐明MiR205Hg在体外和体内实验中的作用；
Barrett的食管（BE）是食管腺癌（EAC）的前体，较长的非编码RNA（LNCRNA）被确定为生物学途径的关键调节剂。在BE和EAC的发展中；体内和（3）的体内实验涉及刺猬（HH）信号通路的MiR205HG的机制。抑制小鼠的异种移植肿瘤生长vivo. Finally, we show that one mechanism of action of miR205HG involves the Hh signaling pathway: miR205HG and Hh expression levels were inversely correlated in both EAC (r = −0.73) and BE (r = −0.83) tissues, and in vitro studies revealed details of Hh signaling inhibition induced by miR205HG. In conclusion, these findings establish that lncRNA miR205HG functions as a tumor suppressor in the development of BE and EAC，至少部分通过其对HH信号通路的影响。
Barrett’s esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC). Long noncoding RNAs (lncRNAs) have been identified as key regulators of biological pathways and we identified lncRNA, miR205HG, as a tumor suppressor in the development of Barrett’s esophagus and esophageal adenocarcinoma, in part through its effect on the Hedgehog signaling pathway. The aims of the current study were: (1) to study involvement of miR205HG in the development of BE and EAC (2) to clarify the role of miR205HG in in vitro and in vivo experiments; and (3) to investigate the mechanism of miR205HG involving the Hedgehog (Hh) signaling pathway Barrett’s esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC). Recently, long noncoding RNAs (lncRNAs) have been identified as key regulators of biological pathways. However, involvement of lncRNAs in the development of BE and EAC has not been well-studied. The aims of the current study were: (1) to study involvement of the lncRNA, miR205HG, in the development of BE and EAC; (2) to clarify the role of miR205HG in in vitro and in vivo experiments; and (3) to investigate the mechanism of miR205HG involving the Hedgehog (Hh) signaling pathway. These experiments revealed that miR205HG was downregulated in EAC vs. normal esophageal epithelia (NE) as well as in EAC cell lines, and its forced overexpression inhibited EAC cell proliferation and cell cycle progression in vitro. Similarly, overexpression of miR205HG inhibited xenograft tumor growth in mice In vivo. Finally, we show that one mechanism of action of miR205HG involves the Hh signaling pathway: miR205HG and Hh expression levels were inversely correlated in both EAC (r = −0.73) and BE (r = −0.83) tissues, and in vitro studies revealed details of Hh signaling inhibition induced by miR205HG. In conclusion, these findings establish that lncRNA miR205HG functions as a tumor suppressor in the development of BE and EAC, at least in part through its effect on the Hh signaling pathway.
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