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 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 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.

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 CircRNA circPDSS1 promotes bladder cancer by down-regulating miR-16

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Qinnan Yu ◽  
Pei Liu ◽  
Guangye Han ◽  
Xiangdong Xue ◽  
Derong Ma
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Circular Rna ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Migration Rates ◽  
Urothelial Bladder ◽  
And Migration

Abstract Background: Circular RNA (circRNA) circPDSS1 is a recently identified oncogene in gastric cancer, while its roles in other types of cancer are unknown. We investigated the functions of circPDSS1 in urothelial bladder cancer (UBC). Materials and methods: Seventy-two patients (50 males and 22 females, age 38–69 years, mean: 52.3 ± 6.3 years) with UBC were enrolled in Gansu Provincial People’s Hospital from August 2015 to August 2018. RT-qPCR was used to measure gene expression levels in both biopsies from UBC patients and in vitro cultivated HT-1197 and UMUC3 cells. Cell transfections were performed to analyze gene interactions. Cell proliferation, transwell migration and invasion assays were performed to analyze the effects of transfections on HT-1197 and UMUC3 cell proliferation, migration and invasion, respectively. Results: We found that circPDSS1 was up-regulated in UBC. Expression levels of circPDSS1 were increased with increase in clinical stages. MiR-16 was down-regulated and correlated with circPDSS1 in UBC. Overexpression of circPDSS1 led to down-regulation of miR-16, while miR-16 overexpression failed to significantly affect circPDSS1. Overexpression of circPDSS1 led to increased proliferation, invasion and migration rates of UBC cells. Overexpression of miR-16 not only led to inhibited proliferation, invasion and migration of UBC cells, but also attenuated the effects of circPDSS1 overexpression. Conclusion: Therefore, circRNA circPDSS1 may promote UBC by down-regulating miR-16.

Role of integrins in cell invasion and migration

2002 ◽  
Vol 2 (2) ◽  
pp. 91-100 ◽  
Author(s):  
John D. Hood ◽  
David A. Cheresh
Keyword(s):  
Cell Invasion ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Expression of Talin-1 in endometriosis and its possible role in pathogenesis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xian Tang ◽  
Qing Li ◽  
Lijie Li ◽  
Jianfa Jiang
Keyword(s):  
Cell Invasion ◽  
Expression Level ◽  
Migration And Invasion ◽  
Endometrial Stromal Cells ◽  
Invasion And Migration ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression ◽  
Polymerase Chain ◽  
And Migration

Abstract Background Endometriosis is a disease that involves active cell invasion and migration. Talin-1 can promote cell invasion, migration and adhension in various cancer cells, but its role in endometriosis has not been investigated. This study was to investigate the expression level of Talin-1 in endometriosis and the role of Talin-1 in the proliferation, adhesion, migration, and invasion of human endometrial stromal cells (ESCs). Methods Ectopic and eutopic endometrial tissues were collected from women with endometriosis, and the control endometrial tissues were obtained from patients without endometriosis. The expression level of Talin-1 was detected in each sample using quantitative real-time polymerase chain reaction and immunohistochemistry. The expression of Talin-1 was inhibited using RNA interference in ESCs, and its proliferation, apoptosis, adhesion, migration, and invasion capacity were analyzed. Western blotting was performed to detect the expression of related molecules after the downregulation of Talin-1. Results The results showed that the mRNA and protein expression of Talin-1 were significantly increased in the ectopic endometrium and eutopic endometrial tissues compared with the controls. The knockdown of Talin-1 did not affect the proliferation and apoptosis of ESCs. The results indicated that the downexpression of Talin-1 inhibited the adhesion, invasion, and migration of ESCs. In addition, the expressions of N-cadherin, MMP-2, and integrin β3 were significantly lower after the deregulation of Talin-1, whereas the levels of E-cadherin were significantly increased. Conclusions The expression of Talin-1 was increased in the ectopic and eutopic endometrial tissues compared with the control endometrium. The downregulation of Talin-1 inhibited the adhesion, invasion, and migration of ESCs.

scholarly journals LncRNA PSMG3-AS1 Downregulates miR-340 through Methylation to Upregulate ROCK1 and Promote Cell Invasion and Migration in Non-small Cell Lung Cancer

2021 ◽  
Author(s):  
Xiyong Wang ◽  
Yang Yang ◽  
Yu Dai ◽  
Hongming Zhang ◽  
Honglin Xia ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Mirna Gene ◽  
Small Cell ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
And Migration

Abstract Background: LncRNA PSMG3‑AS1 plays oncogenic role in breast cancer. However, its role in non-small cell lung cancer (NSCLC) is hardly known. We then studied the role of PSMG3‑AS1 in NSCLC.Methods: RT-qPCR was performed to determine the expression of PSMG3‑AS1 in NSCLC and non-tumor tissues from 60 NSCLC patients. A survival analysis was carried out to visit patients for 5 years to study the role PSMG3‑AS1 in prediction the survival of NSCLC. NSCLC cells were overexpressed with miR-340 or PSMG3‑AS1 to analyze the crosstalk between PSMG3‑AS1 and miR-340. MSP was performed to analyze the methylation of miR-340 miRNA gene. The invasion and migration abilities of cells were determind by Transwell assays.Results: PSMG3‑AS1 was highly expressed in NSCLC and was closely correlated poor survival. PSMG3‑AS1 and miR340 were inversely correlated. In NSCLC cells, PSMG3‑AS1 decreased the expression of miR-340 and increased methylation of miR-340 gene. However, miR-340 overexpression did not significantly affect the expression of PSMG3‑AS1. In addition, PSMG3‑AS1 overexpression resulted in upregulated expression of ROCK1. PSMG3‑AS1 and ROCK1 overexpression increased cell invasion and migration rates. MiR-340 overexpression suppressed cell behaviors and inhibited the role of PSMG3‑AS1.Conclusions: PSMG3‑AS1 may downregulate miR-340 through methylation to upregulate ROCK1 and promote cell invasion and migration in NSCLC.

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