scholarly journals LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Xing Peng ◽  
Jinyu Gao ◽  
Chunyan Cai ◽  
Yumei Zhang
Keyword(s):  
Cervical Cancer ◽  
Molecular Mechanism ◽  
Target Gene ◽  
Critical Role ◽  
Downstream Target ◽  
Cell Proliferation And Migration ◽  
Downstream Target Gene ◽  
And Migration ◽  
Proliferation And Migration

Abstract Cervical cancer (CC), an aggressive malignancy, has a high risk of relapse and death, mainly occurring in females. Accumulating investigations have confirmed the critical role of long noncoding RNAs (lncRNAs) in diverse cancers. LncRNA LINC01503 has been reported as an oncogene in several cancers. Nonetheless, its role and molecular mechanism in CC have not been explored. In the present study, we found that FXYD3 expression was considerably up-regulated in CC tissues and cells. Moreover, FXYD3 deficiency conspicuously hampered cell proliferation and migration while facilitated cell apoptosis in CC cells. Subsequently, molecular mechanism experiments implied that FXYD3 was a downstream target gene of miR-342-3p, and FXYD3 expression was reversely mediated by miR-342-3p. Moreover, we discovered that LINC01503 acted as the endogenous sponge for miR-342-3p. Besides, LINC01503 negatively regulated miR-342-3p expression and positively regulated FXYD3 expression in CC. Rescue assays revealed that LINC01503 depletion-induced repression on CC progression could be partly recovered by miR-342-3p inhibition, and then the co-transfection of sh-FXYD3#1 rescued this effect. Conclusively, LINC01503 aggravated CC progression through sponging miR-342-3p to mediate FXYD3 expression, providing promising therapeutic targets for CC patients.

scholarly journals E2F6-Mediated Downregulation of MIR22HG Facilitates the Progression of Laryngocarcinoma by Targeting the miR-5000-3p/FBXW7 Axis

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Hui Chen ◽  
Mudunov Ali ◽  
Azizyan Ruben ◽  
Dimitry Stelmakh ◽  
Maksim Pak
Keyword(s):  
Cell Proliferation ◽  
Target Gene ◽  
Noncoding Rnas ◽  
Downstream Target ◽  
Cell Proliferation And Migration ◽  
Abundant Evidence ◽  
Downstream Target Gene ◽  
And Migration ◽  
Proliferation And Migration

ABSTRACT Recently, abundant evidence has clarified that long noncoding RNAs (lncRNAs) play an oncogenic or anticancer role in the tumorigenesis and development of diverse human cancers. Described as a crucial regulator in some cancers, MIR22HG has not yet been studied in laryngocarcinoma and therefore the underlying regulatory role of MIR22HG in laryngocarcinoma is worth detecting. In this study, MIR22HG expression in laryngocarcinoma cells was confirmed to be downregulated, and upregulated MIR22HG expression led to suppressive effects on laryngocarcinoma cell proliferation and migration. Molecular mechanism assays revealed that MIR22HG sponges miR-5000-3p in laryngocarcinoma cells. Besides, decreased expression of miR-5000-3p suppressed laryngocarcinoma cell proliferation and migration. Moreover, the FBXW7 gene was reported to be a downstream target gene of miR-5000-3p in laryngocarcinoma cells. More importantly, rescue assays verified that FBXW7 depletion or miR-5000-3p upregulation countervailed the repressive effects of MIR22HG overexpression on laryngocarcinoma progression. In addition, E2F6 was proved to be capable of inhibiting MIR22HG transcription in laryngocarcinoma cells. To sum up, E2F6-induced downregulation of MIR22HG promotes laryngocarcinoma progression through the miR-5000-3p/FBXW7 axis.

miR-375 Affects the Proliferation, Invasion, and Apoptosis of HPV16-Positive Human Cervical Cancer Cells by Targeting IGF-1R

2016 ◽  
Vol 26 (5) ◽  
pp. 851-858 ◽  
Author(s):  
Xiao Yu ◽  
Weihong Zhao ◽  
Xin Yang ◽  
Zhilian Wang ◽  
Min Hao
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Gene ◽  
Negative Control ◽  
Expression Level ◽  
Cell Proliferation And Migration ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

ObjectiveThe aim of this study was to examine the relationship between miR-375 expression and the proliferation, apoptosis, and migration of cervical cancer cells. To further explore the potential target gene of miR-375, insulin-like growth factor 1 receptor (IGF-1R) was detected in miR-375 overexpressed and inhibited cervical cancer cells, which clarified the potential mechanism of miR-375 in the growth and development of cervical cancer.MethodsIn a cervical cancer cell line (Caski), miR-375 overexpression and knockdown were achieved by transfection with a synthetic miR-375 mimic or miR-375–targeting inhibitor oligonucleotides, respectively, using siRNA-Mate transfection reagents. Real-time Polymerase Chain Reaction was performed to detect the expression level of miR-375. The functional effects of miR-375 on cell proliferation, migration, and apoptosis were evaluated using a Cell Counting Kit (CCK-8) and through scratch wound tests and apoptosis assays, respectively. Western blotting was performed to detect the expression level of the IGF-1R protein.ResultTransfection with the miR-375 mimic significantly upregulated the expression of miR-375 by approximately 7.76-fold (P< 0.05), reduced cell proliferation and migration (P< 0.05), increased apoptosis (P< 0.05), and decreased the expression of the IGF-1R protein by 24.73% (P< 0.05) compared with the negative control. In contrast, transfection of the miR-375 inhibitor decreased the expression of miR-375 by 14.39% (P< 0.05), significantly increased cell proliferation and migration (P< 0.05), significantly reduced the cell apoptosis (P< 0.05), and upregulated the expression of the IGF-1R protein by 2.29-fold (P< 0.05). The cells transfected with the negative control showed no significant changes compared with the blank control for each parameter (P> 0.05).ConclusionsmiR-375 plays an important role in the tumorigenesis and development of cervical cancer. IGF-1R might represent a target gene of miR-375 in cervical cancer.

scholarly journals miR-425-5p Acts as a Molecular Marker and Promoted Proliferation, Migration by Targeting RNF11 in Hepatocellular Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Dan Rao ◽  
Songmei Guan ◽  
Junwei Huang ◽  
Qing Chang ◽  
Shigang Duan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Malignant Tumors ◽  
Inhibitory Effect ◽  
Malignant Progression ◽  
Downstream Target ◽  
Downstream Target Gene ◽  
And Migration ◽  
The Relationship ◽  
Proliferation And Migration

Hepatocellular carcinoma (HCC) is one of the most common and dangerous malignant tumors in China, which causes a large number of deaths every year. MicroRNAs (miRNAs) dysfunction contributes to the malignant progression of tumors. The aim of our study was to investigate the relationship between the biological role of miR-425-5p and malignant progression of HCC. Our results showed that miR-425-5p expression was significantly upregulated in HCC tissues and closely related to the poor prognosis of HCC patients. The knockdown of miR-425-5p inhibited cell proliferation and migration. Further, we identified RNF11 as the downstream target gene of miR-425-5p. In addition, the rescue experiments showed that the upregulation of RNF11 could rescue the inhibitory effect of miR-425-5p on HCC. In general, miR-425-5p as an oncogene promotes the malignant development of HCC via RNF11 and serves as a molecular target for predicting the prognosis of HCC patients.

Exosomal miR-214-5p Released from Glioblastoma Cells Modulates Inflammatory Response of Microglia after Lipopolysaccharide Stimulation through Targeting CXCR5

2019 ◽  
Vol 18 (1) ◽  
pp. 78-87 ◽  
Author(s):  
Jian-kai Yang ◽  
Hong-jiang Liu ◽  
Yuanyu Wang ◽  
Chen Li ◽  
Ji-peng Yang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Clinical Prognosis ◽  
Direct Target ◽  
And Migration ◽  
High Level ◽  
Cxcr5 Expression ◽  
Proliferation And Migration

Background and Objective: Exosomes communicate inter-cellularly and miRNAs play critical roles in this scenario. MiR-214-5p was implicated in multiple tumors with diverse functions uncovered. However, whether miR-214-5p is mechanistically involved in glioblastoma, especially via exosomal pathway, is still elusive. Here we sought to comprehensively address the critical role of exosomal miR-214-5p in glioblastoma (GBM) microenvironment.Methods:The relative expression of miR-214-5p was determined by real-time PCR. Cell viability and migration were measured by MTT and transwell chamber assays, respectively. The secretory cytokines were measured with ELISA kits. The regulatory effect of miR-214-5p on CXCR5 expression was interrogated by luciferase reporter assay. Protein level was analyzed by Western blot.Results:We demonstrated that miR-214-5p was aberrantly overexpressed in GBM and associated with poorer clinical prognosis. High level of miR-214-5p significantly contributed to cell proliferation and migration. GBM-derived exosomal miR-214-5p promoted inflammatory response in primary microglia upon lipopolysaccharide challenge. We further identified CXCR5 as the direct target of miR-214- 5p in this setting.Conclusion:Overexpression of miR-214-5p in GBM modulated the inflammatory response in microglia via exosomal transfer.

Abstract 2178: Sonic Hedgehog In Adult Hypoxic Cerebellum

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Giuseppe Straface ◽  
Andrea Flex ◽  
Federico Biscetti ◽  
Eleonora Gaetani ◽  
Giovanni Pecorini ◽  
...  
Keyword(s):  
Sonic Hedgehog ◽  
Target Genes ◽  
Positive Staining ◽  
Lacz Gene ◽  
Downstream Target ◽  
Shh Pathway ◽  
And Migration ◽  
First Time ◽  
Proliferation And Migration

Background: Cerebellar hypoxia is responsible for important aspects of cognitive deterioration and motor disturbances in neurological disorders, such as stroke, vascular dementia, and neurodegeneration. In the cerebellum, VEGF is significantly upregulated after hypoxia and is able to induce angiogenesis, reduce neuronal apoptosis, and regulate neuronal differentiation, proliferation, and migration. But, VEGF is not sufficient to provide neuroprotection. A crucial role is played by growth associated protein-43 (GAP43), for which important activities have been described. The purpose of this study was to investigate the role of the developmental Sonic hedgehog (Shh) signaling pathway in postnatal hypoxic cerebellum and its relationship with VEGF and GAP43 expression. Methods: We used adult C57BL/6J mice, ptc1-lacZ mice, and GAP43−/− mice for these experiments. Ptc1-lacZ mice carry a non-disruptive insertion of the lacZ gene under the control of the ptc1 promoter. Ptc1 is a downstream-transcriptional target of Shh and its upregulation indicates activation of the Shh pathway. Mice were exposed to systemic normobaric hypoxia (6%O 2 ) for 6 hours and the expression of Shh, Ptc1, VEGF, and GAP43 were investigated. Results: After exposure to hypoxia, Shh-positive staining was detected in Purkinje cells (PCs). The same cells were also lacZ(ptc1)-positive, indicating that PCs are both Shh-producing and -responding elements. Also the cells of the internal granular layer (IGL) were lacZ(ptc1)-positive, indicating that these cells are Shh-responsive. LacZ(ptc1)-positive IGL cells were also immunopositive for VEGF and GAP-43. We also found that ptc1 expression is lost in PCs of GAP43−/− mice, indicating that Shh requires GAP43 to activate its downstream target genes in PCs. Finally, when cultures enriched in granular cells were stimulated with Shh recombinant protein, GAP43 phosphorylation was increased. This effect was inhibited by Shh-inhibitor cyclopamine. Conclusions: This is the first time that hypoxia is reported to activate the Shh pathway in the adult. Our data suggest that the Shh pathway might be important for the cerebellar response to hypoxia, through interactions with VEGF and GAP43.

scholarly journals Role of Anillin in Tumour: From a Prognostic Biomarker to a Novel Target

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1600
Author(s):  
Nguyen Minh Tuan ◽  
Chang Hoon Lee
Keyword(s):  
Prognostic Biomarker ◽  
Tumour Microenvironment ◽  
Vital Role ◽  
Actin Binding ◽  
Cell Proliferation And Migration ◽  
Novel Target ◽  
And Migration ◽  
The Impact ◽  
Proliferation And Migration

Anillin (ANLN), an actin-binding protein, reportedly plays a vital role in cell proliferation and migration, particularly in cytokinesis. Although there have been findings pointing to a contribution of ANLN to the development of cancer, the association of ANLN to cancer remains not fully understood. Here, we gather evidence to determine the applicability of ANLN as a prognostic tool for some types of cancer, and the impact that ANLN has on the hallmarks of cancer. We searched academic repositories including PubMed and Google Scholar to find and review studies related to cancer and ANLN. The conclusion is that ANLN could be a potent target for cancer treatment, but the roles ANLN, other than in cytokinesis and its influence on tumour microenvironment remodeling in cancer development, must be further elucidated, and specific ANLN inhibitors should be found.

scholarly journals Biological and Clinical Significance of the CCR5/CCL5 Axis in Hepatocellular Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 883 ◽  
Author(s):  
Santosh K. Singh ◽  
Manoj K. Mishra ◽  
Brian M. Rivers ◽  
Jennifer B. Gordetsky ◽  
Sejong Bae ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Clinical Significance ◽  
Treatment Options ◽  
Biological Significance ◽  
Improve Patient Survival ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Despite the improvement in survival for patients with liver cancer (LCa) in recent decades, only one in five patients survive for 5 years after diagnosis. Thus, there is an urgent need to find new treatment options to improve patient survival. For various cancers, including LCa, the chemokine CCL5 (RANTES) facilitates tumor progression and metastasis. Since the function of the CCR5/CCL5 interaction in LCa cell proliferation and migration is poorly understood, the present study was undertaken to investigate the role of the CCR5/CCL5 axis in these processes. Flow cytometry, RT-PCR, Western blot, and immunofluorescence techniques were used to quantify the expression of CCR5 and CCL5 in LCa cells. To determine the biological significance of CCR5 expressed by LCa cell lines, a tissue microarray of LCas stained for CCR5 and CCL5 was analyzed. The results showed higher expression (p < 0.001) of CCR5 and CCL5 in hepatocellular carcinoma (HCC) tissues compared to non-neoplastic liver tissues. Furthermore, to delineate the role of the CCR5/CCL5 interaction in LCa cell proliferation and migration, various LCa cells were treated with maraviroc, a CCR5 antagonist, in the presence of CCL5. These data demonstrated the biological and clinical significance of the CCR5/CCL5 axis in LCa progression. The targeting of this axis is a promising avenue for the treatment of LCa.

scholarly journals MicroRNA-23a promotes colorectal cancer cell migration and proliferation by targeting at MARK1

2019 ◽  
Vol 51 (7) ◽  
pp. 661-668 ◽  
Author(s):  
Xiaoli Tang ◽  
Meiyuan Yang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Daorong Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Functional Role ◽  
Expression Level ◽  
Colorectal Cancer Cell ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract The functional role of microRNA-23a in tumorigenesis has been investigated; however, the exact mechanism of microRNA-23a (miR-23a) in colorectal cancer development has not been fully explored. In the present study, we aimed to investigate the molecular functional role of miR-23a in colorectal carcinogenesis. Quantitative real-time polymerase chain reaction was conducted to investigate the expression level of miR-23a in tissue samples and cell lines (HCT116 and SW480). CCK-8, colony formation and Transwell assay were used to explore the role of miR-23a in cell proliferation and migration. Dual luciferase reporter assay was used to identify the direct binding of miR-23a with its target, MARK1. Western blot analysis was used to analyze the expression level of MARK1, as well as a confirmed miR-23a target gene, MTSS1, in miR-23a-mimic and miR-23a-inhibit groups. Rescue experiments were conducted by overexpression of MARK1 in miR-23a-mimic-transfected cell lines. The results showed that miR-23a was highly expressed in colorectal cancer tissue and cell lines. MiR-23a could promote proliferation and migration of colorectal cancer cell lines. MARK1 was a direct target of miR-23a and the expression level of MARK1 was down-regulated in miR-23a-mimic-transfected cell lines but up-regulated in miR-23a-inhibit-transfected cells. Overexpression of MARK1 could partly reverse the cancer-promoting function of miR-23a. Our results suggested that miR-23a promotes colorectal cancer cell proliferation and migration by mediating the expression of MARK1. MiR-23a may be a potential therapeutic target for colorectal cancer treatment.

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