XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p.
XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p.
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DOI：
10.3349/ymj.2018.59.7.816
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发表时间：
2018-09
影响因子：
2.4
通讯作者：
Wu W
中科院分区：
文献类型：
--
作者：
Lin XQ;Huang ZM;Chen X;Wu F;Wu W
X染色体失活特异性转录本（XIST）和XIST附近的X染色体失活相关长链非编码RNA（lncRNA）对肝细胞癌（HCC）的影响在以往的研究中仍存在争议，本研究旨在验证这一点。DIANA lncRNA-microRNA（miRNA）相互作用数据库用于探索miRNA与JPX或XIST的相互作用。通过RT-qPCR分析配对HCC标本和相邻正常组织中的JPX、XIST和miR-155- 5 p表达水平。通过双荧光素酶报告基因测定验证XIST与miR-155- 5 p之间的相互作用。通过RT-qPCR和Western blot在有或没有XIST敲入的HepG 2细胞中验证miR-155- 5 p及其已知靶基因SOX 6和PTEN的表达水平。XIST和JPX对HCC的潜在抑制作用通过使用异种移植模型的细胞功能测定和肿瘤形成测定来验证。与邻近组织相比，HCC病理标本中JPX和XIST表达显著降低，这与HCC进展和miR-155- 5 p表达增加相关。双荧光素酶报告基因分析显示XIST是miR-155- 5 p的直接靶点。XIST敲入显著降低miR-155- 5 p表达水平，增加SOX 6和PTEN表达水平，同时显著抑制HepG 2细胞体外生长，miR-155- 5 p模拟物转染可部分逆转该抑制作用。JPX基因敲入显著增加XIST表达，并以XIST依赖性方式抑制体外HepG 2细胞生长或体内肿瘤形成。JPX和XIST在HCC中起抑制作用。JPX增加了HCC细胞中XIST的表达水平，其通过海绵状吸收促进miR-155- 5 p的癌症来抑制HCC的发展。
The influence of X-inactive specific transcript (XIST) and X-chromosome inactivation associated long non-coding RNAs (lncRNAs) just proximal to XIST (JPX) on hepatocellular carcinoma (HCC) remains controversial in light of previous reports, which the present study aimed to verify. The DIANA lncRNA-microRNA (miRNA) interaction database was used to explore miRNA interactions with JPX or XIST. JPX, XIST, and miR-155-5p expression levels in paired HCC specimens and adjacent normal tissue were analyzed by RT-qPCR. Interaction between XIST and miR-155-5p was verified by dual luciferase reporter assay. Expression levels of miR-155-5p and its known target genes, SOX6 and PTEN, were verified by RT-qPCR and Western blot in HepG2 cells with or without XIST knock-in. The potential suppressive role of XIST and JPX on HCC was verified by cell functional assays and tumor formation assay using a xenograft model. JPX and XIST expression was significantly decreased in HCC pathologic specimens, compared to adjacent tissue, which correlated with HCC progression and increased miR-155-5p expression. Dual luciferase reporter assay revealed XIST as a direct target of miR-155-5p. XIST knock-in significantly reduced miR-155-5p expression level and increased that of SOX6 and PTEN, while significantly inhibiting HepG2 cell growth in vitro, which was partially reversed by miR-155-5p mimic transfection. JPX knock-in significantly increased XIST expression and inhibited HepG2 cell growth in vitro or tumor formation in vivo in a XIST dependent manner. JPX and XIST play a suppressive role in HCC. JPX increases expression levels of XIST in HCC cells, which suppresses HCC development by sponging the cancer promoting miR-155-5p.
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影响因子：
13.5
作者：
Wang, Bo;Majumder, Sarmila;Nuovo, Gerard;Kutay, Huban;Volinia, Stefano;Patel, Tushar;Schmittgen, Thomas D.;Croce, Carlo;Ghoshal, Kalpana;Jacob, Samson T.
通讯作者：
Jacob, Samson T.
癌症中的长非编码 RNA：信号传导电路。
影响因子：
19
作者：
Lin C;Yang L
通讯作者：
Yang L
影响因子：
28.2
作者：
Karreth FA;Pandolfi PP
通讯作者：
Pandolfi PP
长非编码RNA XIST通过调节非小细胞肺癌中的miR-367/141-ZEB2轴促进TGF-β诱导的上皮间质转化
影响因子：
9.7
作者：
Li, Chang;Wan, Liang;Zhang, Hong-Tao
通讯作者：
Zhang, Hong-Tao
DOI：
10.1016/j.clinre.2016.09.002
发表时间：
2017-03-01
影响因子：
2.7
作者：
Ma, Weijie;Wang, Haitao;Yuan, Yufeng
通讯作者：
Yuan, Yufeng