scholarly journals Dicer1 Promotes Colon Cancer Cell Invasion and Migration Through Modulation of tRF-20-MEJB5Y13 Expression Under Hypoxia

2021 ◽  
Vol 12 ◽  
Author(s):  
Na Luan ◽  
Yali Mu ◽  
Jiayi Mu ◽  
Yiquan Chen ◽  
Xun Ye ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Cell Invasion ◽  
Underlying Mechanism ◽  
Therapeutic Interventions ◽  
Invasion And Migration ◽  
Hypoxic Conditions ◽  
Non Coding Rna ◽  
Cell Progression ◽  
And Migration

Hypoxia plays a key role in colorectal cancer (CRC) metastasis, but its underlying mechanism remains largely unknown. Dicer1, an RNase, has been considered as a tumor regulator in many tumors. However, whether Dicer1 affects CRC progression under hypoxia remains uncertain. In this study, we found that Dicer1 expression was induced by hypoxia in CRC cells and it mediates hypoxia-induced CRC cell progression. Furthermore, we found that the expression of tRF-20-MEJB5Y13, a small non-coding RNA derived from tRNA, was increased under hypoxic conditions, and its upregulation by Dicer1 resulted in hypoxia-induced CRC cell invasion and migration. These results advance the current understanding of the role of Dicer1 in regulating hypoxia signals and provide a new pathway for the development of therapeutic interventions for inhibiting cancer progression.

scholarly journals LncRNA-MALAT1-mediated Axl promotes cell invasion and migration in human neuroblastoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769979 ◽  
Author(s):  
Shaojie Bi ◽  
Chunyan Wang ◽  
Yixin Li ◽  
Wei Zhang ◽  
Juan Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Invasion ◽  
Neuroblastoma Cells ◽  
Great Influence ◽  
Regulatory Mechanisms ◽  
Human Neuroblastoma ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Overexpression of Axl has been noted to correlate with several human cancers. However, the regulatory mechanisms and effects of Axl in human neuroblastoma development remain unclear. Here, we explore the expression of Axl in neurobalstoma and related upstream regulatory mechanisms of invasion and migration. We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1. Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. Furthermore, we found that targeting Axl by inhibitor R428 significantly suppressed the abilities of tumor cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.

scholarly journals Long Non-Coding RNA-DUXAP8 Regulates TOP2A in the Growth and Metastasis of Osteosarcoma via MicroRNA-635

2020 ◽  
Author(s):  
Ting Yang ◽  
Jian Ping Quo ◽  
Fan Li ◽  
Chao Xiu ◽  
Hua Wang ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Human Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Real Time Quantitative Pcr ◽  
Diagnosis And Prognosis ◽  
Non Coding Rna ◽  
Cell Progression ◽  
And Migration

Abstract Purpose: Osteosarcoma (OS) is a malignant tumor disease with high morbidity and mortality in children and adolescents. Evidence indicates that long non-coding RNAs (lncRNAs) may be important players in human cancer progression, including OS. In this study, we identified the role of lnc-DUXAP8 in the development of OS.Materials and Methods: Expression of lncRNA DUXAP8 was determined by real-time quantitative PCR and Western blotting in OS tissues. Cell proliferation was evaluated using CCK8 and colony formation assay; Transwell assay was conducted to measure cell invasion. Cell migration was evaluated using Wound Healing assay. The binding site between the lnc-DUXAP8 and miR-635 RNAs was evaluated using a luciferase reporter assay. Results: The expression of the lnc-DUXAP8 was significantly upregulated in OS samples and OS cell lines compared to normal tissue. High expression of lncRNA DUXAP8 was associated with shorter overall survival. Knockdown of lncRNA DUXAP8 inhibited proliferation and migration, and invasion in OS cells. More importantly, mechanism investigation revealed that lncRNA DUXAP8 was predominantly acted as a competing endogenous RNA (ceRNA) in OS by regulating miR-635/ TOP2A axis. Conclusion: LncRNA DUXAP8 is upregulated in OS, and LncRNA DUXAP8 knockdown plays a vital anti-tumor role in OS cell progression through a miR-635/ TOP2A axis. Our study suggests that LncRNA DUXAP8 may be a novel, promising biomarker for diagnosis and prognosis of OS.

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 miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Mingli Suo ◽  
Yanfei Sun ◽  
Hailan Yang ◽  
Jing Ji ◽  
Yinfang He ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Cell Invasion ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
And Migration

Abstract Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE.

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 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 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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