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LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/?-catenin signaling pathway.

ABSTRACT: BACKGROUND:Endothelial-to-mesenchymal transition (EndMT) plays significant roles in atherosclerosis, but the regulatory mechanisms involving lncRNAs remain to be elucidated. Here we sort to identify the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in ox-LDL-induced EndMT. METHODS:The atherosclerosis model was established by feeding ApoE-/- mice with high-fat diet, and the levels of lncRNA MALAT1 in mouse arterial tissue were detected by RT-qPCR. Cell model was established by treating human umbilical vein endothelial cells (HUVECs) with ox-LDL, and the levels of EndMT markers, such as CD31, vWF, ?-SMA and Vimentin and lncRNA MALAT1 levels were detected and their correlations were analyzed. The role of MALAT1 in EndMT and its dependence on Wnt/?-catenin signaling pathway was further detected by knocking down or overexpressing MALAT1. RESULTS:MALAT1 was upregulated in high-fat food fed ApoE-/- mice. HUVECs treated with ox-LDL showed a significant decrease in expression of CD31 and vWF, a significant increase in expression of ?-SMA and vimentin, and upregulated MALAT1. An increased MALAT1 level facilitated the nuclear translocation of ?-catenin induced by ox-LDL. Inhibition of MALAT1 expression reversed nuclear translocation of ?-catenin and EndMT. Moreover, overexpression of MALAT1 enhanced the effects of ox-LDL on HUVEC EndMT and Wnt/?-catenin signaling activation. CONCLUSIONS:Our study revealed that the pathological EndMT required the activation of the MALAT1-dependent Wnt/?-catenin signaling pathway, which may be important for the onset of atherosclerosis. TRIAL REGISTRATION:Not applicable.

SUBMITTER: Li H

PROVIDER: S-EPMC6417088 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/β-catenin signaling pathway.

Li Hongrong H Zhao Qifei Q Chang Liping L Wei Cong C Bei Hongying H Yin Yujie Y Chen Meng M Wang Hongtao H Liang Junqing J Wu Yiling Y

Lipids in health and disease 20190314 1

<h4>Background</h4>Endothelial-to-mesenchymal transition (EndMT) plays significant roles in atherosclerosis, but the regulatory mechanisms involving lncRNAs remain to be elucidated. Here we sort to identify the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in ox-LDL-induced EndMT.<h4>Methods</h4>The atherosclerosis model was established by feeding ApoE<sup>-/-</sup> mice with high-fat diet, and the levels of lncRNA MALAT1 in mouse arterial tissue were detected by RT-qPC ...[more]

PMID: 30871555

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Project description:BackgroundStudies have shown that cancer susceptibility candidate 11 (CASC11), a newly discovered long non-coding RNA (lncRNA), was aberrantly overexpressed in hepatic carcinoma, gastric cancer and colorectal cancer. However, its effects on cervical cancer has been kept unknown up to now. The present study was aimed to investigate the relationship between lncRNA CASC11 and cervical cancer and further explore the mechanism of CASC11 effect on cervical cancer progression.MaterialsQuantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of CASC11 in cancerous and adjacent normal tissues of patients with cervical cancer as well as in cell lines. The proliferation, migration, invasion and apoptosis were assayed after transfecting the cell with si-CASC11 or pcDNA3.1-CASC11. TOP/FOP-Flash luciferase reporter assay and western blot were used to analysis the activation of Wnt/β-catenin signaling pathway. Si-CASC11-transfected HeLa cells were subcutaneously inoculated into male athymic (nude) mice to investigate the effect of CASC11 on the tumor formation.ResultsWe discovered that CASC11, the expression of which was positively associated with the tumor size and the FIGO staging and negatively related to the patients' survival rate, was up-regulated in the cervical cancer tissues and cell lines. Silencing CASC11 inhibited the proliferation, migration as well as invasion and promoted the cell apoptosis. Conversely, overexpression of CASC11 facilitated the cancer cell's proliferation, migration and invasion ability and suppressed the apoptosis. Further study showed that CASC11 promoted the migration and invasion of cervical cancer cells by activating Wnt/β-catenin signaling pathway and silencing CASC11 inhibited the tumor growth in vivo.ConclusionOur study demonstrated that CASC11 promoted the cervical cancer progression by activating Wnt/β-catenin signaling pathway for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for cervical cancer.

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LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/?-catenin signaling pathway.

Publications

LncRNA MALAT1 modulates ox-LDL induced EndMT through the Wnt/β-catenin signaling pathway.

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