LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.
LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.
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DOI:
10.3724/abbs.2023227
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发表时间:
2023-10-25
影响因子:
3.7
通讯作者:
Li X
中科院分区:
文献类型:
--
作者:
Xu S;Cheng Z;Du B;Diao Y;Li Y;Li X
AP000695.2 is a novel long non-coding RNA (lncRNA). Its aberrant high expression is remarkably associated with poor prognosis of patients with lung adenocarcinoma (LUAD). However, its role and underlying mechanism in LUAD remains unclear. Previous bioinformatics analysis indicated that AP000695.2 may be closely related to the glycolysis of LUAD. This study aims to verify and explore the mechanism of AP000695.2 in glycolysis of LUAD. Overexpression plasmid and siRNA are used to construct cell models of upregulation and downregulation of AP000695.2, respectively. AP000695.2 is highly expressed in lung cancer cell lines as revealed by qPCR. Western blot analysis, FDG uptake, lactate production assay and ECAR determination results show that high expression of AP000695.2 facilitates glycolysis of LUAD cells. CCK-8, EdU staining, Transwell and wound healing assays show that high expression of AP000695.2 promotes cell growth and migration of LUAD. The relationship between AP000695.2 and miR-335-3p is confirmed by bioinformatics analysis and dual-luciferase reporter assays. Through the dual-luciferase reporter assay, TEA domain transcription factor 1 (TEAD1) is identified as a target gene of miR-335-3p. Rescue experiments are applied to verify the relationship among AP000695.2, miR-335-3p and TEAD1. Our study indicates that AP000695.2 is involved in the mechanism of LUAD through functioning as a ceRNA to competitively sponge miR-335-3p, thereby regulating the expression of TEAD1. In the in vivo models, AP000695.2 depletion restrains tumor growth and glycolysis. AP000695.2 promotes the glycolysis of LUAD by regulating the miR-335-3p/TEAD1 axis, and it may serve as a potential target of anti-tumor energy metabolism therapy.
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DOI:
10.1038/nrc.2017.99
发表时间:
2018-01
期刊:
Nature reviews. Cancer
影响因子:
--
作者:
Anastasiadou E;Jacob LS;Slack FJ
通讯作者:
Slack FJ
影响因子:
5
作者:
通讯作者:
--
影响因子:
8
作者:
Li Y;Liu M;Yang S;Fuller AM;Karin Eisinger-Mathason TS;Yang S
通讯作者:
Yang S
影响因子:
0.9
作者:
He C;Yin H;Zheng J;Tang J;Fu Y;Zhao X
通讯作者:
Zhao X
影响因子:
5.6
作者:
Wang, Liang;Sun, Jin;Lou, Weihua
通讯作者:
Lou, Weihua