LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction <em>via</em> miR-3194-5p regulating JAK1/STAT3 signaling pathway

Abstract

Vascular endothelial cell (VEC) dysfunction is associated with the development of coronary heart disease (CHD). Long intergenic non-protein coding RNA 926 (LINC00926), a kind of long noncoding RNA (lncRNA), has been found to be abnormally expressed in CHD patients. However, the biological role of LINC00926 has not been reported. In our research, we intended to explore the regulatory mechanism of LINC00926 in hypoxia-exposed HUVEC cells (HUVECs). In our in vitro study, HUVECs were exposed under hypoxic conditions (5% O2) for 24 h. RT-qPCR and Western blotting assay were used to detect the mRNA and protein levels. CCK-8 assay, flow cytometry, transwell assay and in vitro angiogenesis assay were performed to measure cell proliferation, apoptosis, migration and tube formation, respectively. Bioinformatics analysis was applied to predict the target of LINC00926 and miR-3194-5p, which was verified by dual-luciferase reporter assays. The results showed that LINC00926 was highly expressed in CHD patients and hypoxia-exposed HUVECs. LINC00926 overexpression suppressed cell proliferation, migration and tube formation and increased cell apoptosis. MiR-3194-5p was a target of LINC00926 and can target binding to JAK1 3’UTR. LINC00926 could up-regulate JAK1 and p-STAT3 levels via miR-3194-5p. In addition, overexpressed LINC00926 suppressed cell proliferation, migration and tube formation and increased cell apoptosis via miR-3194-5p/JAK1/STAT3 axis. In summary, LINC00926 aggravated endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway in hypoxia-exposed HUVECs.

Screening and identification of immunoinfiltrating genes associated with the prognosis and construction of the regulatory axis of competitive endogenous RNA of hepatocellular carcinoma

“…In addition, they can also serve as miRNA sponges to disturb target mRNA mediated by miRNA to resolve. Thereinto, Bam et al found in their research on post-traumatic stress disorder that LINC00926 controls the expression of IFNG and IL17A through physical interactions with MLL1, suggesting that LINC00926 regulates the expression of WNT10B and thereby regulates in ammation [26].Jiang et al found that linc00926 regulates the JAK1/STAT3 signaling pathway through miR-3194-5p, inhibits cell proliferation, migration, and tube formation, and increases cell apoptosis, thereby participating in hypoxia induced vascular endothelial cell dysfunction [27].Linc00861 was found to be a potential intervention target for immunotherapy in prostate cancer patients, which is signi cantly correlated with PD-1 and CTLA4 [28]. In the study of uterine cancer, it was found that the LINC00861/miR-513b-5p axis may inhibit the EMT process of cancer cells through the PTEN/AKT/mTOR signaling pathway [29].The overexpression of linc00294 signi cantly alleviates LPS induced survival inhibition and in ammatory damage in human umbilical vein endothelial cells (HUVECs) [30].In addition, our study found that mir5195 is co-expressed with 17 genes.…”

Paeoniflorin inhibits colorectal cancer cell stemness through the miR‐3194‐5p/catenin beta‐interacting protein 1 axis

“…In addition, miR‐590‐5p expression was markedly reduced in CRC, and its overexpression suppressed the malignant behaviors of cancer cells 10 . A previous study showed that miR‐3194‐5p knockdown suppressed the proliferation, migration, and tube formation of hypoxia‐treated vascular endothelial cells and increased cell apoptosis 11 . Young et al demonstrated that the estradiol‐mediated inhibition of SP1 decreased miR‐3194‐5p expression, promoting lung cancer progression 12 .…”

“…10 A previous study showed that miR-3194-5p knockdown suppressed the proliferation, migration, and tube formation of hypoxia-treated vascular endothelial cells and increased cell apoptosis. 11 Young et al demonstrated that the estradiolmediated inhibition of SP1 decreased miR-3194-5p expression, promoting lung cancer progression. 12 In addition, Hufbauer et al revealed that miR-3194-5p was highly expressed in primary human papillomavirus type 16 oropharyngeal squamous-cell-carcinoma and matched metastasis.…”