scholarly journals miR-210 regulates vascular endothelial cell apoptosis in arteriosclerosis obliterans through the JAK1-STAT3 pathway

2021 ◽  
Author(s):  
Songjie Hu ◽  
Zhongjian Xu ◽  
Dehai Lang
Keyword(s):  
Vascular Endothelial Cell ◽  
Flow Cytometric Analysis ◽  
Janus Kinase ◽  
Luciferase Reporter ◽  
Transcriptional Level ◽  
Vascular Endothelial ◽  
Arteriosclerosis Obliterans ◽  
Qrt Pcr ◽  
Gene Assay ◽  
Huvec Proliferation

IntroductionAtherosclerosis is a continuously worsening chronic condition that starts in the arteries and may then affect other blood vessels. There is increasing evidence linking microRNAs to the development of arteriosclerosis obliterans (ASO). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was applied in this study to detect miR-210-5p (miR-210) expression, and significant upregulation was observed in human arterial walls where ASO was prevalent.Material and methodsThe proliferation of human umbilical vascular endothelial cells (HUVECs) with various levels of miR-210 expression was assessed via MTT and colony-formation assays. Cell proliferation was significantly promoted in HUVECs with upregulated miR-210 levels and reduced in HUVECs with downregulated miR-210 levels.ResultsFlow cytometric analysis of cells stained with annexin V-FITC and propidium iodide data demonstrated that miR-210 inhibited apoptosis, while miR-210 inhibition promoted apoptosis by mediating pro-apoptotic protein expression levels. These results were verified using a dual-luciferase reporter gene assay system, which showed that Janus kinase 1 (JAK1) was directly targeted by miR-210, while an miR-210 mimic significantly decreased downstream JAK1 and signal transducer and activator of transcription 3 (STAT3) activation at a post-transcriptional level in HUVECs, as detected by western blotting and qRT-PCR. Further inhibition of either JAK1 or STAT3 counteracted the effect of miR-210 on HUVEC proliferation and apoptosis. These findings suggest that miR-210 promotes HUVEC proliferation, at least in part, by targeting the JAK1-STAT3 signaling axis.ConclusionsThis study provides insights into the contribution of the miR-210-JAK1-STAT3 axis and its underlying mechanisms to ASO pathology.

scholarly journals miRNA-544a Regulates the Inflammation of Spinal Cord Injury by Inhibiting the Expression of NEUROD4

2018 ◽  
Vol 51 (4) ◽  
pp. 1921-1931 ◽  
Author(s):  
Lei Yang ◽  
Dawei Ge ◽  
Xi Chen ◽  
Chunzhi Jiang ◽  
Shengnai Zheng
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Grip Strength ◽  
Target Gene ◽  
Interleukin 1 ◽  
Luciferase Reporter ◽  
Interleukin 17 ◽  
Qrt Pcr ◽  
Gene Assay ◽  
Cord Injury

Background/Aims: To explore the potential role of miR-544a in spinal cord injury and the possible mechanism involved. Methods: We established a mouse model with spinal cord injury to examine the changes in grip force recovery of the forelimb or the posterior limb of the mouse. Microarray was performed to achieve differentiated miRNAs in the mice. The expressions of miR-544a, MCP-1, IL36B and IL17B after spinal cord injury were detected by qRT-PCR. Subsequently, miR-544a was overexpressed to observe changes in inflammation and grip strength after spinal cord injury. Target gene of miR-544a was then predicted using bioinformatics technology. Finally, dual luciferase reporter gene assay was used to verify the binding of miR-544a to its target gene. Results: Using mice models with spinal cord injury, we found that the strength of their four limbs began to recover 7 days after injury. The results of microarray and qRT-PCR confirmed that mir-544a level in mice with spinal cord injury decreased with increase of injury time, while the levels of inflammatory genes MCP-1 (monocyte chemoattractant protein-1), IL1 (interleukin-1) and TNF-α (tumor necrosis factor alpha) IL36B (interleukin-36 beta) and IL17B (interleukin-17 beta) were significantly increased. However, overexpression of miR-544a in the mice significantly reduced the level of inflammation and restored their grip strength in their four limbs. Finally, we found that miR-544a can bind to the NEUROD4 (Neurogenic differentiation 4) 3’UTR (Untranslated Region) region through bioinformatics website prediction, which was further confirmed by dual luciferase reporter assay. NEUROD4 level was significantly reduced following the overexpression of miR-544a. Conclusion: The expression of miR-544a was significantly decreased after spinal cord injury. High expression of miR-544a could alleviate the inflammation caused by spinal cord injury and promote the recovery of spinal cord via the inhibition of NEUROD4.

scholarly journals Hsa-miR-105-1 Regulates Cisplatin-Resistance in Ovarian Carcinoma Cells by Targeting ANXA9

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Xinxin Kou ◽  
Hui Ding ◽  
Lei Li ◽  
Hongtu Chao
Keyword(s):  
Ovarian Carcinoma ◽  
Cell Lines ◽  
Target Gene ◽  
Molecular Mechanisms ◽  
Cisplatin Resistance ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Qrt Pcr ◽  
Gene Assay ◽  
Increased Sensitivity

Purpose. Cisplatin is one of the most effective drugs for treating ovarian carcinoma (OC), which is among the most lethal types of carcinoma. However, the chemoresistance to cisplatin that develops over time leads to a poor clinical outcome for many OC patients. Therefore, it is necessary to clearly understand the molecular mechanisms of chemoresistance. In this study, we examined how Hsa-miR-105-1 functions in cisplatin-resistant OC cells. Methods. The levels of Hsa-miR-105-1 expression in cisplatin-sensitive and resistant OC cell lines were detected by qRT-PCR. The target gene of Hsa-miR-105-1 was predicted by using the TargetScan and Starbase databases and verified by the double luciferase reporter gene assay. The target gene of Hsa-miR-105-1 was identified as ANXA9, and ANXA9 expression was evaluated by qRT-PCR, western blotting, and immunofluorescence. To validate the function of Hsa-miR-105-1 in OC cells, we silenced or overexpressed Hsa-miR-105-1 in cisplatin-sensitive or resistant OC cell lines, respectively. Furthermore, the expression levels of several apoptosis-related proteins, including P53, P21, E2F1, Bcl-2, Bax, and caspase-3, were examined by western blot analysis. Results. The levels of Hsa-miR-105-1 expression were abnormally downregulated in cisplatin-resistant OC cells, while ANXA9 expression was significantly upregulated in those cells. Treatment with an Hsa-miR-105-1 inhibitor promoted the expression of ANXA9 mRNA and protein, enhanced the resistance to cisplatin, and attenuated the cell apoptosis induced by cisplatin in cisplatin-sensitive OC cells. Moreover, treatment with Hsa-miR-105-1 mimics inhibited ANXA9 expression, which further increased the levels of P53, P21, and Bax expression and decreased the levels of E2F1 and Bcl-2 expression, finally resulting in an increased sensitivity to cisplatin in cisplatin-resistant OC cells. Conclusion. We found that a downregulation of Hsa-miR-105-1 expression enhanced cisplatin-resistance, while an upregulation of Hsa-miR-105-1 restored the sensitivity of OC cells to cisplatin. The Hsa-miR-105-1/ANXA9 axis plays an important role in the cisplatin-resistance of OC cells.

scholarly journals MiR-486 protects against acute myocardial infarction via regulation of PTEN

2021 ◽  
Vol 20 (9) ◽  
pp. 1845-1853
Author(s):  
Qinfeng Han ◽  
Zhong Xu ◽  
Xiaolei Zhang ◽  
Kun Yang ◽  
Zhifei Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Akt Signaling ◽  
Reporter Gene Assay ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Akt Signaling Pathway ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Qrt Pcr ◽  
Gene Assay

Purpose: To investigate the effect of miR-486 on rats with acute myocardial infarction (AMI), and its mechanism of action.Methods: A rat model of AMI was established. They were randomly divided into 4 groups, namely, sham, model, agomiR-486 and antagomiR-486 groups, respectively. Rats in these different groups were treated with agomiR-21 (5 μL, 40 nmol/mL), antagomiR-21 (5 μL, 40 nmol/mL) or agomiR-NC (5 μL, 40 nmol/mL), respectively. Then, key miRNAs were sorted out using gene-chip assay and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Luciferase reporter gene assay was conducted to determine the interaction between miR-486 and gene of PTEN. After intraperitoneal injection of agomiR-486 and antagomiR-486, hemodynamics was measured to determine the effect of miR-486 on myocardial function of the rats. The effect of miR-486 expression level on the expression of myocardial enzymes in serum, the morphology of myocardial tissues, and the apoptosis of myocardial tissues in rats, were investigated. Additionally, the effect of miR-486 expression level on PTEN/AKT signaling pathway in the rats was determined by Western blotting.Results: The results of gene-chip and qRT-PCR assays revealed that there were 8 differentially expressed genes in rat myocardial tissues in the model group when compared with the sham group. MiR-486 improved the cardiac function of rats and the morphology of myocardial tissues, but reduced AMI-induced apoptosis of myocardial cells and the expression of myocardial enzymes (markers of myocardial injury) in a dose-dependent manner (p < 0.05). The results of luciferase reporter gene assay showed that PTEN was a direct target of miR-486. In rat models of AMI, a raised expression of miR-486 remarkably suppressed the protein expression level of PTEN and up-regulated that of p-AKT/AKT (p < 0.05).Conclusion: MiR-486 protects against AMI in rats probably by targeting PTEN and activating the AKT signaling pathway. The results of the current study may provide new insights for the treatment of AMI.

scholarly journals SMARCB1 Promotes Ubiquitination and Degradation of NR4A3 via Direct Interaction Driven by ROS in Vascular Endothelial Cell Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Bingzheng Lu ◽  
Zhu Zhu ◽  
Longxiang Sheng ◽  
Yuan Li ◽  
Yang Yang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protein Level ◽  
Cell Injury ◽  
Pathological Condition ◽  
Vascular Endothelial Cell ◽  
Direct Interaction ◽  
Glucose Deprivation ◽  
Transcriptional Level ◽  
Protein Abundance ◽  
Vascular Endothelial

Nuclear receptor subfamily 4 group A member 3 (NR4A3) protects the vascular endothelial cell (VEC) against hypoxia stress, whose expression is primarily reported to be governed at a transcriptional level. However, the regulation of NR4A3 in the protein level is largely unknown. Here, we report that NR4A3 protein abundance is decreased immensely in VEC injury induced by reoxygenation after oxygen-glucose deprivation (OGD-R), which is significantly blocked by the administration of the antioxidative steroid TRIOL. Moreover, the notable improvement of NR4A3 and the alleviation of pulmonary endothelial barrier hyperpermeability induced by acute hypobaric hypoxia in cynomolgus monkeys are also observed after TRIOL administration. The overproduction of reactive oxygen species (ROS) decreases NR4A3 protein abundance in VEC under OGD-R condition, which is reversed by TRIOL and N-acetylcysteine (NAC). TRIOL dose-dependently increases the NR4A3 protein level by inhibiting ubiquitination and ubiquitin proteasome system- (UPS-) mediated degradation rather than promoting its transcription. Using yeast two-hybrid screening, we further identify the interaction between NR4A3 and SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1), and the DNA-binding domain of NR4A3 is required for this interaction. Knockdown of SMARCB1 reduces ubiquitination and degradation of NR4A3, suggesting the proubiquitylation effect of this interaction which is enhanced by ROS in VEC injury induced by OGD-R. In summary, our study here for the first time reveals a posttranslational regulation in SMARCB1-mediated NR4A3 protein degradation which is driven by ROS, providing further understanding of the impaired regulation of NR4A3-mediated prosurvival pathways under pathological condition in VEC.

lncRNA KCNQ1OT1 promotes the proliferation, migration and invasion of retinoblastoma cells by upregulating HIF-1α via sponging miR-153-3p

2020 ◽  
Vol 68 (8) ◽  
pp. 1349-1356
Author(s):  
Yujin Wang ◽  
Jixiang Wang ◽  
Hongyan Hao ◽  
Xiangxia Luo
Keyword(s):  
Colony Formation ◽  
Rna Binding ◽  
Hypoxia Inducible Factor ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Tissue Samples ◽  
Qrt Pcr ◽  
Gene Assay

It is reported that lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) is oncogenic in many cancers. This work aimed at probing into its expression and biological functions in retinoblastoma (RB) as well as its regulatory effects on miR-153-3p and hypoxia-inducible factor-1α (HIF-1α). In our study, RB samples in pair were collected, and quantitative real-time PCR (qRT-PCR) was employed for examining the expression levels of KCNQ1OT1, miR-153-3p and HIF-1α. KCNQ1OT1 short hairpin RNAs were transfected into SO-Rb50 and HXO-RB44 cell to inhibit the expression of KCNQ1OT1. The proliferative activity, colony formation ability and apoptosis were examined through cell counting kit-8 assay, colony formation assays, Transwell assay and flow cytometry, respectively. qRT-PCR and western blot analysis were used for analyzing the changes of miR-153-3p and HIF-1α induced by KCNQ1OT1. The regulatory relationships between miR-153-3p and KCNQ1OT1, miR-153-3p and HIF-1α were examined by dual luciferase reporter gene assay and RNA-binding protein immunoprecipitation assay. The results of our study showed that KCNQ1OT1 expression was markedly enhanced in RB tissue samples, and KCNQ1OT1 knockdown had an inhibitory effect on the proliferation, migration, invasion and viability of RB cells. There were two validated binding sties between KCNQ1OT1 and miR-153-3p, and KCNQ1OT1 negatively regulated the expression of miR-153-3p in RB cells. HIF-1α was a target gene of miR-153-3p, and could be positively regulated by KCNQ1OT1. In conclusion, our study indicates that KCNQ1OT1 can increase the malignancy of RB cells via regulating miR-153-3p/HIF-1α axis.

Vitamin D Promotes Vascular Endothelial Cell Function via the Regulation of miR-199a-5p

2019 ◽  
Vol 9 (12) ◽  
pp. 1662-1669
Author(s):  
Lianman He ◽  
Yong Wang ◽  
Min Liu ◽  
Ling Li
Keyword(s):  
Vitamin D ◽  
Endothelial Cell ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
Cell Counting ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Vascular Endothelial ◽  
Endothelial Cell Function ◽  
The Impact

Essential hypertension (EH) is a main risk factor for cardiovascular disease. Vitamin D (VD) levels are inversely related to hypertension. MicroRNAs (miRNA or miR) are involved in various diseases, including EH. Till now, the role of miR-199a-5p in EH remains unclear. Cell counting kit-8, flow cytometry and Transwell assay were carried out in the current study to study the effects of VD on the biological behavior of Human umbilical vein endothelial cells (HUVECs). The expression of miR-199a-5p was subsequently determined using reverse transcription-quantitative (RT-q) PCR. TargetScan prediction and double luciferase reporter gene detection were applied to confirm the binding sites between Sirtuin 1 (SIRT1) and miR-199a-5p. The results showed that VD promoted the proliferation and migration of HUVECs and reduced cell apoptosis. VD was observed to significantly reduced miR-199a-5p level in HUVECs. Transfection of the miR-199a-5p mimic was indicated to reverse the influence of VD on the proliferation, migration and apoptosis of HUVECs. SIRT1 was also confirmed to be a target gene of miR-199a-5p. Western blot analysis and RT-qPCR were performed to measure the impact of VD on the SIRT1/AMP-activated protein kinase (AMPK)- /NFB pathway. The results demonstrated that VD increased SIRT1 expression and p-AMPK- and decreased the expression of p-p65, and the transfection of miR-199a-5p mimic reversed these effects. In conclusion, the results of the current study indicated that VD may relieve EH through promoting vascular endothelial cell function via regulating miR-199a-5p.

scholarly journals Circ_0000005 Facilitates Proliferation, Apoptosis, Migration and Invasion of Acute Myeloid Leukemia Cells via Modulating miR-139-5p/Tspan3 Axis

2020 ◽  
Author(s):  
Juan Tong ◽  
Huilan Liu ◽  
Changcheng Zheng ◽  
Xiaoyu Zhu ◽  
Xiang Wan ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Lines ◽  
Reporter Gene ◽  
Reporter Gene Assay ◽  
Luciferase Reporter ◽  
Regulatory Function ◽  
Luciferase Reporter Gene ◽  
Luciferase Reporter Gene Assay ◽  
Qrt Pcr ◽  
Gene Assay

Abstract Background: Accumulating circular RNAs (circRNAs) are reported to be abnormally expressed in diverse cancers, hematologic malignancies included. This study aimed to investigate the biological function and underlying mechanisms of circ_0000005 in acute myeloid leukemia (AML).Materials and methods: Bone marrow samples were enrolled from AML patients with normal samples as controls. Circ_0000005, miR-139-5p and tetraspanin 3 (Tspan3) were detected by qRT-PCR and Western blot, respectively. AML cell lines (KG1 and HL60) were used as cell models. CCK-8, Transwell and flow cytometry assays were adopted to study the biological functions of circ_0000005 on AML cells in vitro. The interrelation between circ_0000005 and miR-139-5p was detected by bioinformatics, qRT-PCR, luciferase reporter gene assay, RNA pull-down assay, and RNA-binding protein immunoprecipitation (RIP) assays. Ultimately, Western blot, qRT-PCR, luciferase reporter gene assay were adopted to corroborate the interrelation between miR-139-5p and its target Tspan3. Results: Circ_0000005 was demonstrably elevated in both AML clinical samples and cell lines. Circ_0000005 overexpression promoted the viability, migration and invasion of AML cells, and repressed the apoptosis of AML cells, while silencing circ_0000005 showed opposite biological effects. Circ_0000005 interacted with miR-139-5p and repressed its expression, and Tspan3 was proved to be negatively regulated by miR-139-5p. Circ_0000005 could promote the expression of Tspan3 via repressing miR-139-5p, and the oncogenic functions of circ_0000005 were dependent on its regulatory function on miR-139-5p/Tspan3 axis.Conclusion: Circ_0000005 facilitates the malignant phenotypes of AML cells via miR-139-5p/Tspan3 axis. Circ_0000005 may serve as a potential therapeutic target in AML.

scholarly journals COX2 Enhances Neovascularization of Inflammatory Tenocytes Through the HIF-1α/VEGFA/PDGFB Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Bin Deng ◽  
Pu Xu ◽  
Bingyu Zhang ◽  
Qing Luo ◽  
Guanbin Song
Keyword(s):  
Growth Factor ◽  
Trichostatin A ◽  
Critical Role ◽  
Tendon Injuries ◽  
Luciferase Reporter ◽  
Inflammatory Factor ◽  
Vascular Endothelial ◽  
Expression Levels ◽  
Transcriptional Targets ◽  
Gene Assay

Tendon injuries are among the most challenging in orthopedics. During the early tendon repair, new blood vessel formation is necessary. However, excessive angiogenesis also exacerbates scar formation, leading to pain and dysfunction. A significantly worse outcome was associated with higher expression levels of hypoxia-inducible factor-1 alpha (HIF-1α), and its transcriptional targets vascular endothelial growth factor A (VEGFA) and platelet-derived growth factor B (PDGFB), but the underlying molecular mechanisms remain unclear. In this study, lipopolysaccharide (LPS) was used to induce an inflammatory response in tenocytes. LPS increased the tenocytes’ inflammatory factor COX2 expression and activated the HIF-1α/VEGFA/PDGFB pathway. Moreover, the conditioned medium from the tenocytes boosted rat aortic vascular endothelial cell (RAOEC) angiogenesis. Furthermore, Trichostatin A (TSA), an inhibitor of histone deacetylase, was used to treat inflammatory tenocytes. The expression levels of HIF-1α and its transcriptional targets VEGFA and PDGFB decreased, resulting in RAOEC angiogenesis inhibition. Finally, the dual-luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay proved that the HIF-1α/PDGFB pathway played a more critical role in tenocyte angiogenesis than the HIF-1α/VEGFA pathway. TSA could alleviate angiogenesis mainly through epigenetic regulation of the HIF-1α/PDGFB pathway. Taken together, TSA might be a promising anti-angiogenesis drug for abnormal angiogenesis, which is induced by tendon injuries.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2020 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract Background: Gastric cancer (GC) is one of the most frequent malignant digestive tumors and second fatal cancer. This study was to investigate whether lncRNA-H19 can regulate E2F3 expression through competitive binding to microRNA-194 (miR-194), thus regulating GC growth and metastasis. Methods: H19, miR-194, and E2F3 expression levels in GC tissues and cell lines were investigated using quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR). Meanwhile, the mRNA levels of H19 and E2F3 in gastric cancer tissues were also analyzed through the GEPIA web tool. The binding condition of miR-194 with H19 and E2F3 was investigated using a dual-luciferase reporter gene assay. The regulatory effects of H19 on proliferative, migratory, and invasive abilities of AGS cells and SGC-7901 cells were detected by transwell assay and cell counting kit-8 (CCK-8). Genes involved in proliferation, migration, and invasion (PCNA, Vimentin, and N-cadherin) were determined using QRT-PCR and western blot. The regulatory interaction between H19 and miR-194, miR-194, and E2F3 were investigated using rescue experiments. Results: The results revealed that H19 was highly expressed in GC tissues and cell lines than those of controls. Downregulated H19 decreased the proliferation, migration, and invasion of AGS cells and SGC-7901 cells. H19 was demonstrated that being the molecular sponge of miR-194 in regulating the growth of the GC cells. The level of E2F3 expression was also found significantly higher in GC tissues and cell lines than those of controls. And then, the mimics of miR-194 inhibited the expression of E2F3 in the GC cells. CCK-8 assay showed decreased proliferative ability induced by miR-194 mimics were reversed by E2F3 overexpression. Transwell assays showed decreased migratory and invasive ability induced by miR-194 mimics were reversed by E2F3 overexpression. Conclusions: This study demonstrates that H19 promotes GC growth and metastasis by regulating E2F3 via competitive binding to miRNA-194.

LncRNA MCM3AP-AS1 promotes proliferation, migration and invasion of oral squamous cell carcinoma cells via regulating miR-204-5p/FOXC1

2020 ◽  
Vol 68 (7) ◽  
pp. 1282-1288
Author(s):  
Hui Li ◽  
Junhong Jiang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Gene Assay

Oral squamous cell carcinoma (OSCC) is a lethal malignancy. It is reportedly demonstrated that long non-coding RNA (lncRNA) participates in the development of OSCC. The purpose of this study was to clarify the function and possible molecular mechanisms of lncRNA MCM3AP antisense RNA 1 (lncRNA MCM3AP-AS1) in OSCC. Quantitative real-time PCR (qRT-PCR) was adopted to investigate MCM3AP-AS1 expressions in OSCC tissues and cells. The proliferation, migration and invasion of HN-6 and SCC-9 cells were probed by cell counting kit-8 and Transwell assays, respectively. Dual luciferase reporter gene assay, Pearson’s correlation analysis, qRT-PCR and western blot were used to detect the binding relationship among miR-204-5 p, MCM3AP-AS1 and forkheadbox C1 (FOXC1). MCM3AP-AS1 expression was elevated in OSCC tissues and cell lines. Overexpression of MCM3AP-AS1 facilitated the proliferation, migration and invasion of OSCC cells, while the knockdown of MCM3AP-AS1 suppressed these malignant phenotypes. Besides, MCM3AP-AS1 impeded miR-204-5 p by binding with it. MCM3AP-AS1 could also upregulate the expression of FOXC1 via repressing miR-204-5 p.MCM3AP-AS1 promotes the progression of OSCC cells by adsorbing miR-204-5 p and upregulating FOXC1 expressions.

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