Upregulation of LINC00659 expression predicts a poor prognosis and promotes migration and invasion of gastric cancer cells.
Upregulation of LINC00659 expression predicts a poor prognosis and promotes migration and invasion of gastric cancer cells.
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DOI:
10.3892/ol.2021.12818
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发表时间:
2021-07
期刊:
影响因子:
2.9
通讯作者:
Fan H
中科院分区:
文献类型:
--
作者:
Gong P;Xu Y;Liu M;Shen X;Mao Y;Li Y;Zhang K;Yu S;Fan H
Long non-coding RNAs (lncRNAs) serve an important role in the progression of cancer. LINC00659 was recently identified as a novel oncogenic lncRNA involved in colon cancer cell proliferation via modulating the cell cycle. However, the function of LINC00659 in other types of cancer, especially in gastric cancer (GC), remains unknown. In the present study, bioinformatics analysis combined with cell experiments were performed to explore the function of LINC00659 in GC. It was revealed that LINC00659 expression was significantly upregulated in GC tissues and cell lines. Increased levels of LINC00659 were associated with advanced tumor stage and unfavorable prognosis of patients with GC. Additionally, upregulated LINC00659 expression promoted the migration and invasion of GC cells. Further analysis using a bioinformatics method revealed that matrix metalloproteinase 15 and IQ motif-containing GTPase activating protein 3 were potential downstream targets of LINC00659 involved in tumor metastasis, although the precise underlying mechanism requires further exploration.
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影响因子:
4
作者:
Nasrollahzadeh-Khakiani, Mojdeh;Emadi-Baygi, Modjtaba;Nikpour, Parvaneh
通讯作者:
Nikpour, Parvaneh
影响因子:
37.3
作者:
Liu Z;Chen Z;Fan R;Jiang B;Chen X;Chen Q;Nie F;Lu K;Sun M
通讯作者:
Sun M
DOI:
10.1158/1541-7786.mcr-16-0352
发表时间:
2017-06
期刊:
Molecular cancer research : MCR
影响因子:
--
作者:
Ptashkin RN;Pagan C;Yaeger R;Middha S;Shia J;O'Rourke KP;Berger MF;Wang L;Cimera R;Wang J;Klimstra DS;Saltz L;Ladanyi M;Zehir A;Hechtman JF
通讯作者:
Hechtman JF
影响因子:
11.2
作者:
Bhan A;Soleimani M;Mandal SS
通讯作者:
Mandal SS
影响因子:
64.5
作者:
Rinn, John L.;Kertesz, Michael;Chang, Howard Y.
通讯作者:
Chang, Howard Y.