scholarly journals Circ-ATAD1 is overexpressed in osteosarcoma (OS) and suppresses the maturation of miR-154-5p to increase cell invasion and migration

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jihui Zhou ◽  
Li Xu ◽  
Peng Yang ◽  
Shibang Lin ◽  
Haizhou Huang
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Subcellular Location ◽  
Transwell Assay ◽  
Expression Levels ◽  
Cell Behaviors ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration

Abstract Background Circ-ATAD1 plays an oncogenic role in gastric cancer. However, its roles in other cancers are unclear. We aimed to analyze the role of circ-ATAD1 in osteosarcoma (OS). Methods The expression levels of circ-ATAD1, mature miR-154-5p, and premature miR-154-5p in paired OS and non-tumor tissues from 56 OS patients were determined using RT-qPCR. Nuclear fractionation assay was performed to analyze the subcellular location of circ-ATAD1. The interaction between circ-ATAD1 and premature miR-154-5p was analyzed using RNA pull-down assay. The role of circ-ATAD1 in regulating miR-154-5p maturation was analyzed using RT-qPCR in cells with overexpression. Transwell assays were performed to analyze the roles of circ-ATAD1 and miR-154-5p in regulating OS cell invasion and migration. Results Circ-ATAD1 was overexpressed in OS compared to non-tumor tissues and was detected in the nuclei of OS cells. Mature miR-154-5p, but not premature miR-154-5p, was downregulated in OS tissues compared to non-tumor tissues and was inversely correlated with circ-ATAD1. In OS cells, circ-ATAD1 overexpression decreased the expression of mature miR-154-5p, but not premature miR-154-5p. Transwell assay analysis showed that circ-ATAD1 overexpression increased cell invasion and migration, and mature miR-154-5p overexpression suppressed these cell behaviors. In addition, circ-ATAD1 overexpression reduced the effects of mature miR-154-5p overexpression on cell behaviors. Conclusions Circ-ATAD1 is overexpressed in OS and suppresses miR-154-5p maturation to increase cell invasion and migration.

scholarly journals The MCM3AP-AS1/miR-126/VEGF axis regulates cancer cell invasion and migration in endometrioid carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jie Yu ◽  
Qiqi Fan ◽  
Lingling Li
Keyword(s):  
Cancer Cell ◽  
Cell Invasion ◽  
Migration And Invasion ◽  
Endometrioid Carcinoma ◽  
Expression Levels ◽  
Cell Behaviors ◽  
Invasion And Migration ◽  
Ec Cells ◽  
And Migration

Abstract Background Long non-coding RNA (lncRNA) MCM3AP-AS1 plays an oncogenic role in several malignancies, but its role in endometrioid carcinoma (EC) is unclear. This study was carried out to explore the role of MCM3AP-AS1 in EC. Methods A total of 60 EC patients were enrolled in this study. Expression levels of MCM3AP Antisense RNA 1 (MCM3AP-AS1), microRNA-126 (miR-126), and vascular endothelial growth factor (VEGF) in tissues and transfetced cells were measured by RT-qPCR. Cell transfections were performed to explore the interaction among MCM3AP-AS1, miR-126 and VEGF. Transwell assays were perfromed to evaluate the invasion and migration abilities of HEC-1 cells after transfection. Results MCM3AP-AS1 was upregulated in EC and predicted poor survival. MCM3AP-AS1 directly interacted with miR-126. In EC cells, overexpression of MCM3AP-AS1 and miR-126 did not significantly affect the expression of each other. In addition, overexpression of MCM3AP-AS1 increased the expression levels of VEGF, a target of miR-126. Moreover, overexpression of MCM3AP-AS1 and VEGF increased the migration and invasion rates of EC cells, while overexpression of miR-126 suppressed these cell behaviors. Overexpression of MCM3AP-AS1 attenuated the role of miR-126 in cell invasion and migration. Conclusions Therefore, MCM3AP-AS1 may serve as a competing endogenous RNA (ceRNA) of miR-126 to upregulate VEGF, thereby regulating cancer cell behaviors in EC.

scholarly journals LncRNA DLGAP1-AS2 Suppresses the Maturation of miR-16 to Suppress Cell Invasion and Migration of Ovarian Cancer Cells

2021 ◽  
Author(s):  
Jie Luo ◽  
Yuqiang Zhang ◽  
Ting Zheng ◽  
Yongping Jing ◽  
Rongyu Cao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Invasion ◽  
Precursor Cell ◽  
Ovarian Cancer Cells ◽  
Inhibitory Effects ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration ◽  
Migration Analysis

Abstract Background: This study aimed to explore the role of lncRNA DLGAP1-AS2 in ovarian cancer (OC). Methods: Expression of DLGAP1-AS2, mature miR-16 and miR-16 precursor in paired OC tissues and non-tumor tissues collected from 62 OC patients was determined by RT-qPCR. Correlations were analyzed by Pearson’s correlation coefficient. Overexpression of DLGAP1-AS2 was achieved in OC cell line UWB1.289 to explore the effects of DLGAP1-AS2 overexpression on the expression of mature miR-16 and miR-16 precursor by RT-qPCR. Transwell assays were performed to analyze the role of DLGAP1-AS2 and miR-16 in regulating the invasion and migration of UWB1.289 cells.Results: DLGAP1-AS2 was upregulated in OC and inversely correlated with mature miR-16, but not miR-16 precursor. In OC cells, DLGAP1-AS2 overexpression resulted in downregulated mature miR-16, but failed to significantly affect the expression of miR-16 precursor. Cell invasion and migration analysis showed that DLGAP1-AS2 overexpression reduced the inhibitory effects of miR-16 overexpression on cell invasion and migration.Conclusions: DLGAP1-AS2 may suppress the maturation of miR-16 to suppress cell invasion and migration of OC cells.

scholarly journals LncRNA IUR downregulates ZEB1 by upregulating miR-200 to inhibit prostate carcinoma

2019 ◽  
Vol 51 (11) ◽  
pp. 607-611 ◽  
Author(s):  
Lingjun Sun ◽  
Taowei Chen ◽  
Tao Li ◽  
Jianda Yu
Keyword(s):  
Cell Invasion ◽  
Prostate Carcinoma ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Migration Rates ◽  
Clinical Stages ◽  
And Migration ◽  
Migration Analysis

We in this study investigated the role of imatinib-upregulated lncRNA (IUR) in prostate carcinoma (PC). We observed that IUR was downregulated in PC, and its expression levels decreased with the increase of clinical stages. In PC tissues, microRNA (miR)-200 was positively, while ZEB1 was inversely correlated with IUR. In PC cells, IUR and miR-200 overexpression mediated the downregulated ZEB1. IUR overexpression mediated the upregulation of miR-200, while IUR expression was not significantly affected by miR-200 overexpression. Cell invasion and migration analysis showed that IUR and miR-200 overexpression resulted in decreased invasion and migration rates. ZEB1 overexpression played an opposite role and attenuated the effects of IUR and miR-200 overexpression. Therefore, IUR can downregulate ZEB1 by upregulating miR-200 to inhibit PC cell invasion and migration.

scholarly journals CLIC1 Promotes the Progression of Gastric Cancer by Regulating the MAPK/AKT Pathways

2018 ◽  
Vol 46 (3) ◽  
pp. 907-924 ◽  
Author(s):  
Bo-pei Li ◽  
Yuan-tian Mao ◽  
Zhen Wang ◽  
Ye-yang Chen ◽  
Ye Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Absolute Quantitation ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Akt Phosphorylation ◽  
Erk Phosphorylation ◽  
And Migration

Background/Aims: Chloride intracellular channel 1 (CLIC1), which is a member of the chloride channel protein family, is associated with various human tumors. Recent studies have shown that CLIC1 is involved in the occurrence and development of gastric cancer (GC). However, the exact mechanism remains unclear in GC. Methods: Effects of CLIC1 on the progression of GC in vivo and in vitro and the potential underlying mechanisms have been investigated by analysing 54 patients with GC, as well as human gastric cell lines SGC-7901 and MGC-803, utilizing proteomics, RT-PCR, Western blotting, flow cytometry, Cell invasion and migration assays and xenograft tumor models. Results: Our study shows that CLIC1 knockdown by targeted-siRNA markedly inhibits GC cell invasion and migration and induces apoptosis in vitro. In total, 54 differentially expressed proteins were identified in GC cells SGC-7901 after CLIC1 silencing by isobaric tags for relative isotope labeled and absolute quantitation (iTRAQ) technology, including integrin α1 (ITGα1) and ITGα3. The expression levels of ITGα3, ITGαv, ITGβ1 and Bcl-2 mRNA and protein were decreased significantly in GC cells after CLIC1 knockdown; ITGα1 and Fas were upregulated, but the level of survivin was not significantly different. GC growth and metabolism were decreased in vivo after CLIC1 silencing, but apoptosis was markedly increased. Further study showed that the expression levels of ITGα3, ITGαv and ITGβ1, as well as AKT-phosphorylation, ERK-phosphorylation and p38-phosphorylation, were reduced in vivo after CLIC1 knockdown, while ITGα1 was upregulated. Conclusions: We speculate that CLIC1 may play an important role in the progression of GC, and its mechanism may be related to the regulation of integrin family proteins, which leads to the sequential regulation of the PI3K/AKT, MAPK/ERK and MAPK/p38 pathways.

scholarly journals MENA promotes esophageal squamous cell carcinoma cell invasion and migration via MMP-2, MMP-9 and AKT activation

2020 ◽  
Author(s):  
Yueheng Li ◽  
Na Gao ◽  
Jing Li ◽  
Zhengfan Gao ◽  
Zhenzhen Yang ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Wound Healing Assay ◽  
Transwell Assay ◽  
Invasion And Migration ◽  
Akt Activation ◽  
Qrt Pcr ◽  
And Migration ◽  
Migration Capacity

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is a fatal disease with poor prognosis. The predominant reason for ESCC-related death is metastasis caused by tumor cell invasion. Human MENA protein is a member of Ena/Vasp family, which plays a critical role during tumor cell invasion. However, the biological effect of MENA in ESCC cell lines remains unclear Methods: In this study, fluorescent quantitative real-time PCR (qRT-PCR) were conducted to detect the mRNA expression of MENA in tumor and para-cancer tissue, CCK-8 assay and clone formation assay were conducted to evaluate cell proliferation activity, Transwell assay and wound-healing assay were conducted to detect the changes of cell invasion and migration capacity, siRNA and MENA expression vector were constructed to explore biological function of MENA in ESCC cell lines. Western blot analysis were conducted to detect the expressions of MENA , molecular markers of epithelial-mesenchymal transition (EMT), Akt, p-Akt, MMP-2 and MMP-9 respectively in ESCC cell line. Results: The qRT-PCR experiment results showed that MENA expression in ESCC tissue of 35 patients was relatively higher than that in tissue adjacent to cancer. CCK-8 assay suggested that tumor cell proliferation capacity was suppressed followed by the knockdown of MENA expression in Mena high ESCC cell TE13 and was potentiated by the overexpression of MENA in Mena low ESCC cell TE1. Transwell assay and wound healing assay demonstrated that interfering in MENA could inhibit TE13 cells invasion and migration capacity by affecting the expressions of Matrix metalloproteinase-2(MMP-2) and Matrix metalloproteinase-9 (MMP-9), in contrast, overexpression of MENA in Mena low ESCC cell TE1 could promote invasion and migration by up-regulated expression of MMP-2 and MMP-9. Western blot analysis indicated that interfering of MENA expression could affect EMT-related molecular markers (E-cadherin, N-cadherin, Snail, Slug), Akt and p-Akt Conclusions: Our study reveal that MENA could promote the ESCC cell invasion and migration by upregulate MMP-2, MMP-9 expression and Akt activation. Meanwhile, interfering of MENA expression could affect EMT in ESCC cells. This indicated that MENA may be a potential molecular therapeutic target for ESCC metastasis

The role of circCNIH4 in the adipocyte's effects on metastasis of breast cancer cells.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e13086-e13086
Author(s):  
Xiu Chen ◽  
Jinhai Tang
Keyword(s):  
Breast Cancer ◽  
Wound Healing ◽  
Cell Invasion ◽  
Invasion And Migration ◽  
Non Invasive ◽  
In Vivo Experiments ◽  
And Migration ◽  
Mcf 7

e13086 Background: Obesity is associated with the risk of breast cancer(BCa) incidence and development. However, biological changes in obesity BCa individuals are still uncertain. Nowadays, circCNIH4, one of novel non-coding RNAs, was found to be a non-invasive biomarker in cancers. Methods: We verified the cancer-promoting role of obesity in BCa patients by comparing BMI indexes of 33 BCa and 44 benign tumor patients. Then we cocultured viscera adipose cells(HPA-v) and BCa cells(MCF-7/H and MDA-MB-231/H) to confirm the function of adipocytes on metastasis of BCa cells through wound healing, transwell assays. In vivo experiments were also performed. We analyzed the expression level of circCNIH4 in MCF-7/H, MDA-MB-231/H and different subtypes of BCa cells by quantitative polymerase chain reaction. Simultaneously, we identified inhibited effects of circCNIH4 on metastasis of BCa cells by wound healing, transwell assays and verified the location of circCNIH4 by FISH. Luciferase Assay was used to detect harbored miRNA. Rescue experiments were then applied. Results: We found the BMI of BCa patients(24.37±2.51) was much higher than benign patients(22.97±2.91). Metastasis of BCa cells were obviously promoted after in vitro and in vivo experiments. Then we found the expression of circCNIH4 in MCF-7/H and MDA-MB-231/H were down-regulated 0.71 and 0.52 than that in MCF-7 and MDA-MB-231. Also, circCNIH4 was positively correlated with less aggressive types of BCa cells. Overexpression of circCNIH4 in MDA-MB-231 could suppress cell invasion and migration, while silencing of it in MCF-7 promoted cell invasion and migration. The FISH assay demonstrated that circCNIH4 mainly located in the cytoplasm and might function as a “sponge” for miRNA. MiR-135b functioned as a tumor promoter gene from data of 93 BCa patients (HR = 2.27; 1.01 − 5.12), and it could be captured by circCNIH4 via luciferase and rescued assays. Conclusions: In this study, we revealed that BMI or viscera adipocytes could deteriorate prognosis of BCa and circCNIH4 could be a novel biomarker for non-invasive BCa. In details, circCNIH4 mainly suppressed the adipocyte's pro-metastasis effects on BCa by capturing miR-135b.

scholarly journals Hsa_circ_0013290 Acts as Cancer-Promoting Gene in Hepatocellular Carcinoma

2021 ◽  
Vol 28 ◽  
pp. 107327482110556
Author(s):  
Xi Luo ◽  
Yicun Liu ◽  
Han Li ◽  
Tiaochun Cheng ◽  
Jianjun Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Subcellular Location ◽  
Cell Counting ◽  
Cell Cycle Distribution ◽  
Invasion And Migration ◽  
And Migration ◽  
Hcc Cells

Background As a new class of non-coding RNAs, circRNAs have been recently reported to be involved in the tumorigenesis and progression of human cancers. In the current study, we attempted to explore the potential function of a novel circRNA (hsa_circ_0013290) in hepatocellular carcinoma (HCC). Methods Relative hsa_circ_0013290 expression was analyzed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The subcellular location of hsa_circ_0013290 was performed by RNA subcellular isolation and fluorescence in situ hybridization (FISH) assays. The effect of hsa_circ_0013290 on proliferation was detected by Cell Counting Kit-8 (CCK-8) assays. The effect of hsa_circ_0013290 on cell cycle distribution and apoptosis was detected by flow cytometry. The invasion and migration abilities of hsa_circ_0013290 were detected by transwell assays. Results Hsa_circ_0013290 is significantly upregulated in HCC cell lines and mainly located in cytoplasm of HCC cells. Hsa_circ_0013290 overexpression promotes cell invasion and migration and inhibits cell apoptosis. In contrast, hsa_circ_0013290 knockdown impedes cell invasion and migration and accelerates cell apoptosis. However, hsa_circ_0013290 did not affect cell proliferation. Conclusions Hsa_circ_0013290 is overexpressed in HCC cell lines and is mainly located in the cytoplasm of HCC cells. Hsa_circ_0013290 promotes cell invasion and migration, and inhibits cell apoptosis.

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