LINC02678 as a Novel Prognostic Marker Promotes Aggressive Non-small-cell Lung Cancer.
LINC02678 as a Novel Prognostic Marker Promotes Aggressive Non-small-cell Lung Cancer.
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LINC02678 作为一种新型预后标志物促进侵袭性非小细胞肺癌。
DOI：
10.3389/fcell.2021.686975
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发表时间：
2021
影响因子：
5.5
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Jia D;Xing Y;Zhan Y;Cao M;Tian F;Fan W;Huang J;Cui Y;Gu R;Cui Y;Liu Y;Zhang S;Cai L;Li X
非小细胞肺癌（NSCLC）被认为是一种致命的疾病，其特征是预后不良。据报道，长链非编码RNA（lncRNA）在实体瘤中充当生物标志物和治疗靶标。然而，lncRNA的表达及其在NSCLC中的临床意义仍不确定。采用The Cancer Genome Atlas和Gene Expression Omnibus（GSE 81089）中的基因表达数据来筛选NSCLC中差异表达的lncRNA。发现LINC 02678在NSCLC中上调，并在NSCLC组织中显示启动子区的低甲基化。LINC 02678（也称为RP 11 -336A10.5）与NSCLC患者的总生存期和无复发生存期较差相关。功能获得和丧失的体外模型表明，LINC 02678通过促进NSCLC细胞增殖和细胞周期进展以及诱导NSCLC细胞迁移、侵袭和上皮-间质转化来促进NSCLC进展。LINC 02678主要定位于细胞核中，并可与zeste增强子同源物2（EZH 2）结合。此外，我们发现LINC 02678敲低损害了细胞周期蛋白依赖性激酶抑制剂1B（CDKN 1B）和E-钙粘蛋白启动子区组蛋白3（H3 K27 me 3）上EZH 2的占用能力和赖氨酸27的三甲基化，如ChIP-qPCR所证实的。小鼠移植模型进一步证明LINC 02678可以促进NSCLC细胞的致瘤和转移能力。我们发现LINC 02678在NSCLC中是一种肿瘤促进剂，它通过与EZH 2结合促进NSCLC细胞的生长和转移，表明LINC 02678可能作为癌症诊断和治疗的潜在生物标志物。
Non-small-cell lung carcinoma (NSCLC) is considered to be a fatal disease and characterized by a poor prognosis. Long non-coding RNAs (lncRNAs) have been reported to act as biomarkers and therapeutic targets in solid tumors. However, the expression of lncRNAs and their clinical relevance in NSCLC remain undetermined. The gene expression data profiled in The Cancer Genome Atlas and Gene Expression Omnibus (GSE81089) were employed to screen differentially expressed lncRNAs in NSCLC. LINC02678 was found to be upregulated in NSCLC and exhibited hypomethylation of the promoter region in NSCLC tissues. LINC02678 (also called RP11-336A10.5) was associated with poorer overall survival and relapse-free survival in NSCLC patients. In vitro models of gain- and loss-of-function demonstrated that LINC02678 promotes NSCLC progression by promoting NSCLC cell proliferation and cell cycle progression, as well as inducing NSCLC cell migration, invasion and epithelial-mesenchymal transition. LINC02678 was primarily located in the nucleus and could bind with the enhancer of zeste homolog 2 (EZH2). Moreover, we found that LINC02678 knockdown impaired the occupancy capacity of EZH2 and trimethylation of lysine 27 on histone 3 (H3K27me3) at the promoter region of cyclin dependent kinase inhibitor 1B (CDKN1B) and E-cadherin, as confirmed by ChIP-qPCR. A mouse transplantation model further demonstrated that LINC02678 could promote the tumorigenic and metastatic capacities of NSCLC cells. We identified LINC02678 as a tumor promoter in NSCLC, which enhanced the growth and metastasis of NSCLC cells by binding with EZH2, indicating that LINC02678 may serve as a potential biomarker for cancer diagnosis and treatment.
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影响因子：
64.8
作者：
通讯作者：
--
影响因子：
4
作者：
Orom, Ulf Andersson;Shiekhattar, Ramin
通讯作者：
Shiekhattar, Ramin
影响因子：
11.2
作者：
Bhan A;Soleimani M;Mandal SS
通讯作者：
Mandal SS
CUEDC1 通过 TβRI/Smad 信号通路抑制上皮间质转化，并抑制非小细胞肺癌的肿瘤进展。
DOI：
10.18632/aging.103329
发表时间：
2020-10-25
期刊：
Aging
影响因子：
--
作者：
Cui Y;Song Y;Yan S;Cao M;Huang J;Jia D;Liu Y;Zhang S;Fan W;Cai L;Li C;Xing Y
通讯作者：
Xing Y
影响因子：
11.2
作者：
Hussain M;Rao M;Humphries AE;Hong JA;Liu F;Yang M;Caragacianu D;Schrump DS
通讯作者：
Schrump DS