scholarly journals The Value and Clinical Significance of Tumor Marker Detection in Cervical Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Wei-Li Sun ◽  
Yong Shen ◽  
Yuan Yuan ◽  
Xiao-Jing Zhou ◽  
Wei-Peng Li
Keyword(s):  
Cervical Cancer ◽  
Binding Sites ◽  
Target Genes ◽  
Biological Marker ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Luciferase Reporter Gene ◽  
Downstream Target ◽  
Marker Detection ◽  
Common Malignancy

When it comes to cervical cancer, it is the most common malignancy in gynecology. This study aimed to investigate the concomitant status of miRNA-9-5p in cervical cancer and explore its potential mechanism for treating cervical cancer. The levels of miRNA-9-5p, CA125, CA199, and CEA expression were detected by RT-PCR, and the downstream target genes regulated by miRNA-9-5p were screened by the Venn map. Cytoscape was utilized to find the binding sites of the two genes, and luciferase reporter assay verified the direct regulation of miRNA-9-5p and CXCR4; the CCK-8 assay detected its regulation on cell proliferation, and the expression of miRNA-9-5p, CXCR4, PCNA, Ki67 mRNA, and proteins was detected by RT-PCR and western blot. The expression of miRNA-9-5p was decreased, while the levels of CA125, CA199, and CEA were increased in the model group. The database predicts that CXCR4 is a gene regulated by miRNA-9-5p. The luciferase reporter gene results indicated that miRNA-9-5p could directly regulate the expression of CXCR4 and miRNAs are detected by intracellular transfer inhibitors. In total, MiRNA-9-5p can be utilized as a biological marker for cervical cancer that may inhibit cancer cells’ proliferation by inhibiting the expression of the CXCR4 gene and protein.

scholarly journals miR-126 targeting GOLPH3 inhibits the epithelial-mesenchymal transition of gastric cancer BGC-823 cells and reduces cell invasion

2020 ◽  
Vol 64 (4) ◽  
Author(s):  
Jiancai Ouyang ◽  
Fuhu Song ◽  
He Li ◽  
Rui Yang ◽  
Haicheng Huang
Keyword(s):  
Gastric Cancer ◽  
Target Genes ◽  
Epithelial Mesenchymal Transition ◽  
Cell Model ◽  
Human Tumor ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Luciferase Reporter Gene ◽  
Mesenchymal Transition ◽  
Incidence And Mortality

The incidence and mortality of gastric cancer have been increasing in recent years. MiR-126 and target genes have been studied in gastric cancer, but their studies with Golgi phosphoprotein 3 (GOLPH3) and related pathways in gastric cancer are rarely reported. In the present study, we aimed to investigate the interaction between the miR-126 and GOLPH3in the progression of gastric cancer. In this study, we revealed the role of miR-126-GOLPH3 axis into regulating the progression of epithelial-mesenchymal transition (EMT) in BGC-823 cell model. Firstly, tumor tissues and adjacent normal tissues were collected from 45 patients with gastric cancer. We found the expression of miR-126 in human tumor tissue was significantly lower than in normal tissue using reverse transcription-polymerase chain reaction (RT-PCR). But the GOLPH3 expression was opposite by the detection of immunohistochemistry, RT-PCR and Western blot. Moreover, we predicted miR-126 targeting GOLPH3 by bioinformatics and confirmed the interaction using luciferase reporter gene system; miR-126 inhibited the proliferation, invasion and EMT progression in BGC-823 cells through overexpressing miR-126; miR-126 negative regulated GOLPH3 expression by overexpressing and interfering miR-126. Finally, we found GOLPH3 could promote proliferation using MTT assay, invasion using Transwell, and EMT progression by inhibiting the expression of E-cadherin, inducing vimentin and N-cadherin in BGC-823 cells. Our results demonstrated that miR-126 inhibits proliferative and invasive ability as well as EMT progression by targeting GOLPH3. This study may provide a new field of vision for targeted treatment of gastric cancer.

lag-1, a gene required for lin-12 and glp-1 signaling in Caenorhabditis elegans, is homologous to human CBF1 and Drosophila Su(H)

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1373-1383 ◽  
Author(s):  
S. Christensen ◽  
V. Kodoyianni ◽  
M. Bosenberg ◽  
L. Friedman ◽  
J. Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Binding Sites ◽  
Feedback Loop ◽  
Target Genes ◽  
Sequence Similarity ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Downstream Target ◽  
Binding Factor ◽  
Flanking Regions

The homologous receptors LIN-12 and GLP-1 mediate diverse cell-signaling events during development of the nematode Caenorhabditis elegans. These two receptors appear to be functionally interchangeable and have sequence similarity to Drosophila Notch. Here we focus on a molecular analysis of the lag-1 gene (lin-12 -and glp-1), which plays a central role in LIN-12 and GLP-1-mediated signal transduction. We find that the predicted LAG-1 protein is homologous to two DNA-binding proteins: human C Promoter Binding Factor (CBF1) and Drosophila Suppressor of Hairless (Su(H)). Furthermore, we show that LAG-1 binds specifically to the DNA sequence RTGGGAA, previously identified as a CBF-1/Su(H)-binding site. Finally, we report that the 5′ flanking regions and first introns of the lin-12, glp-1 and lag-1 genes are enriched for potential LAG-1-binding sites. We propose that LAG-1 is a transcriptional regulator that serves as a primary link between the LIN-12 and GLP-1 receptors and downstream target genes in C. elegans. In addition, we propose that LAG-1 may be a key component of a positive feedback loop that amplifies activity of the LIN-12/GLP-1 pathway.

scholarly journals Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shufen Li ◽  
Lifen Zhao ◽  
Xujiong Li ◽  
Gaiping Shang ◽  
Lijing Gao ◽  
...  
Keyword(s):  
A549 Cell ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Cell Damage ◽  
A549 Cells ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Downstream Target ◽  
Apoptosis Related Protein

Objective. To assess whether miR-204 and HA affect A549 cell injury induced by lipopolysaccharide. Material and Methods. A549 cells were treated with hirsutanol A, and cell damage was induced by LPS followed by analysis of cell proliferation by CCK-8, cell apoptosis by flow cytometry, apoptosis-related protein expression by western blot, downstream target of miR-20 by dual-luciferase reporter gene, and inflammatory factors by ELISA and PCR. Results. LPS can significantly inhibit the viability of A549 cells, induce cell apoptosis, and promote the release of IL-6, IL-1β, and TNF-α, while HA pretreatment can target FOXK2 by upregulating miR-204 levels, thereby alleviating apoptosis and promoting cell viability and at the same time inhibiting the release of inflammatory factors by inhibiting the activation of NF-κB. Conclusions. miR-204 participates in the protection of HA acute lung injury by targeting FOXK2.

MiR-30a-5p Downregulation Induces Neuronal Autophagy by Activating AMPK After 2856MHz Microwave Radiation

2021 ◽  
Author(s):  
Yanhui Hao ◽  
Wenchao Li ◽  
Hui Wang ◽  
Jing Zhang ◽  
Haoyu Wang ◽  
...  
Keyword(s):  
Microwave Radiation ◽  
Hippocampal Neurons ◽  
Target Genes ◽  
Neuronal Damage ◽  
Luciferase Reporter ◽  
Potential Health ◽  
Downstream Target ◽  
Neuronal Autophagy

Abstract Background With the development of science and technology, microwaves are being widely used. More and more attention has been paid to the potential health hazards of microwave exposure. The regulation of miR-30a-5p (miR-30a) on autophagy is involved in the pathophysiological process of many diseases. Our previous study found that 30 mW/cm2 microwave radiation could reduce miR-30a expression and activate neuronal autophagy in rat hippocampus. However, the roles played by miR-30a in microwave-induced neuronal autophagy and related mechanisms remain largely unexplored. Results In the present study, we established neuronal damage models by exposing rat hippocampal neurons and rat adrenal pheochromocytoma (PC12) cell-derived neuron-like cells to 30 mW/cm2 microwave, which resulted in miR-30a downregulation and autophagy activation in vivo and in vitro. Bioinformatics analysis was conducted, and Beclin1, Prkaa2, Irs1, Pik3r2, Rras2, Ddit4, Gabarapl2 and autophagy-related gene 12 (Atg12) were identified as potential downstream target genes of miR-30a involved in regulating autophagy. Based on our previous findings that microwave radiation can cause a neuronal energy metabolism disorder, Prkaa2, encoding adenosine 5’-monophosphate-activated protein kinase α2 (AMPKα2, an important catalytic subunit of energy sensor AMPK), was selected for further analysis. Dual-luciferase reporter assay results showed that Prkaa2 is a downstream target gene of miR-30a. Microwave radiation increased the expression and phosphorylation (Thr172) of AMPKα both in vivo and in vitro. Moreover, the transduction of cells with miR-30a mimics suppressed AMPKα2 expression, inhibited AMPKα (Thr172) phosphorylation and reduced autophagy flux in neuron-like cells. Importantly, miR-30a mimics abolished microwave-activated autophagy and inhibited microwave-induced AMPKα (Thr172) phosphorylation. Conclusions AMPKα2 was a newly founded downstream gene of miR-30a involved in autophagy regulation, and miR-30a downregulation after microwave radiation could promote neuronal autophagy by increasing AMPKα2 expression and activating AMPK signaling.

Overexpressed miR-375-Loaded Restrains Development of Cervical Cancer Through Down-Regulation of Frizzled Class Receptor 4 (FZD4) with Liposome Nanoparticle as a Carrier

2021 ◽  
Vol 17 (9) ◽  
pp. 1882-1889
Author(s):  
Suqin Wang ◽  
Lina Xu ◽  
Zhiqiang Zhang ◽  
Ping Wang ◽  
Rong Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
M Phase ◽  
The Impact

Dysregulation expression of miR-375 is noted to correlate with progression of cervical cancer. This study attempted to investigate the impact of overexpressed miR-375-loaded liposome nanoparticles on proliferation of cervical cancer (CC), to provide an insight on pathogenesis of CC disorder. CC cells were co-cultured with pure liposome nanoparticles (empty vector group), miR-375 agonist-loaded liposome nanoparticles, or transfected with miR-375 antagonist. Besides, some cells were exposed to TGF-β/Smads signaling pathway inhibitor or activator whilst cell proliferation was assessed by MTT assay, and expressions of FZD4 and miR-375 were determined. Western blot analysis was carried out to detect the expression of TGF-β pathway factors (TGF-β, Smad2, Smad7, p-Smad2) and its downstream Smads pathway. The interaction between miR-375 and FZD4 was evaluated by dual-luciferase reporter gene assay. Overexpression of miR-375 induced arrest at the G0/G1 phase of cell cycle and elevation of Smad2 protein expression (P <0.05), with lower expressions of TGF-β, Smad7, p-Smad2, and FZD4, while transfection with miR-375 inhibitor exhibited opposite activity. Presence of miR-375 agonist-loaded liposome nanoparticles induced decreased cell proliferation. There was a targeting relationship between miR-375 and FZD4, and administration with TGF-β/Smads agonist resulted in increased miR-375 and Smad2 expressions, as well as decreased TGF-β, Smad7, p-Smad2, FZD4 protein expression, and the number of S phase and G2/M phase cells (P < 0.05). The signaling inhibitor oppositely suppressed cell proliferation decreasing miR-375 expression. miR-375-loaded liposome nanoparticles activated TGF-β/Smads signaling pathway to restrain cell cycle and suppress cell division, and proliferation through targeting FZD4 in CC. Its molecular mechanism is related to activation of TGF-β/Smads signaling pathway.

scholarly journals LINC00511 accelerated the process of gastric cancer by targeting miR-625-5p/NFIX axis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhaosheng Chen ◽  
Honglei Wu ◽  
Zhen Zhang ◽  
Guangchun Li ◽  
Bin Liu
Keyword(s):  
Gastric Cancer ◽  
Binding Sites ◽  
Regulatory System ◽  
Tumor Promoter ◽  
Luciferase Reporter ◽  
Loss Of Function ◽  
Ki67 Expression ◽  
Downstream Target ◽  
Reporter Assays ◽  
Non Coding Rnas

Abstract Background Gastric cancer (GC) is a common-sighted cancer which is hard to cure over the world. Substantial researches revealed that long non-coding RNAs (lncRNAs) were fundamental regulators in the process of cancers. Nevertheless, the biological function of LINC00511 and how LINC00511 was involved in the regulatory system in GC remained unclear. Methods RIP assays and luciferase reporter assays were performed to illustrate combination between LINC00511 and miR-625-5p. Loss-of-function assays were applied for identifying LINC00511 function in GC. Results In our study, LINC00511 was discovered significantly high in expression in GC tissues and cell lines. Moreover, LINC00511 showed a strong expression in I/II and III/IV stage. Knockdown of LINC00511 could inhibit the cell proliferation while enhanced cell apoptosis rate in GC. We used nuclear–cytoplasmic fractionation to judge the subcellular localization of LINC00511. Furthermore, miR-625-5p was found to have binding sites for LINC00511 and negatively regulated by LINC00511. Overexpression of miR-625-5p repressed the course of GC. And knockdown of miR-625-5p could recover the effects of LINC00511 silence. Besides, NFIX was discovered as a downstream target of miR-625-5p and overexpression of NFIX could offset the influence of LINC00511 silence. The results of vivo studies manifested that down-regulation of LINC00511 could reduce the Ki67 expression and NFIX while lifted the expression of miR-625-5p. Conclusion Overall, the results from our study demonstrated that LINC00511 could function as a tumor promoter by targeting miR-625-5p NFIX axis, suggesting LINC00511 could be considered as a target for GC treatment.

scholarly journals LncRNA LINC00460 promotes the papillary thyroid cancer progression by regulating the LINC00460/miR-485-5p/Raf1 axis

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Guangjun Li ◽  
Qingli Kong
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Cancer Progression ◽  
Binding Sites ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Papillary Thyroid ◽  
Potential Biomarker ◽  
Common Malignancy

Abstract Background Papillary thyroid cancer (PTC) is the most common malignancy of all thyroid cancers. LncRNA LINC00460 has been proved to play roles in the oncogenesis and progression of various tumors, including papillary thyroid cancer. However, the potential molecular mechanism of LINC00460 in PTC is poorly investigated. Results LINC00460 was upregulated in PTC tissues and cells. Raf1 was upregulated in PTC tissues, but miR-485-5p was down-regulated. High LINC00460 expression was associated with poor prognosis. LINC00460 knockdown suppressed proliferation, migration, invation and EMT of PTC cells. Bioinformatics prediction revealed that LINC00460 had binding sites with miR-485-5p, which was validated by luciferase reporter assay. In addition, miR-485-5p was confirmed to directly target Raf1 3′-UTR. Moreover, LINC00460 promoted PTC progression by sponging miR-485-5p to elevate the expression of Raf1. Knockdown of LINC00460 restrained tumor growth in vivo. Conclusion LINC00460 induced proliferation, migration, invation and EMT of PTC cells by regulating the LINC00460/miR-485-5p/Raf1 axis, which indicated that LINC00460 may be a potential biomarker and therapeutic target for PTC.

Krüppel-like factor 4 represses transcription of the survivin gene in esophageal cancer cell lines

2009 ◽  
Vol 390 (5/6) ◽  
Author(s):  
Guo Zhang ◽  
Hongxia Zhu ◽  
Yihua Wang ◽  
Shangbin Yang ◽  
Mei Liu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Binding Sites ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Mobility Shift ◽  
Aberrant Expression ◽  
Survivin Gene ◽  
Survivin Promoter

Abstract Aberrant expression of survivin has been shown to be regulated at the transcription level in cancer cells. In this study, we demonstrate that there are six putative binding sites of Krüppel-like factor 4 (KLF4) within the 2000-bp region upstream of the transcription start site of the human survivin gene. Luciferase reporter gene assays revealed that survivin promoter activity is repressed upon overexpression of KLF4 in EC9706 cells. A chromatin immunoprecipitation assay indicated that KLF4 indeed binds the survivin promoter in vivo. It specifically binds the site located at position -40 among the six binding sites as determined by electrophoretic mobility shift assay. Ectopic expression of KLF4 decreases the mRNA and protein levels of survivin. Furthermore, overexpression of survivin partially reverses KLF4-induced cell apoptosis. These results indicate that KLF4 is a transcriptional repressor of the human survivin gene in esophageal squamous cancer cells.

scholarly journals Analyzing the whole-transcriptome profiles of ncRNAs and predicting the competing endogenous RNA networks in cervical cancer cell lines with cisplatin resistance

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Huimin Lv ◽  
Shanshan Jin ◽  
Binbin Zou ◽  
Yuxiang Liang ◽  
Jun Xie ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cervical Cancer ◽  
Reporter Gene ◽  
Biological Function ◽  
Malignant Tumors ◽  
Luciferase Reporter ◽  
Sequencing Analysis ◽  
Luciferase Reporter Gene ◽  
Network Analyses ◽  
Whole Transcriptome

Abstract Background Cervical cancer (CC) is one of the most common malignant tumors in women. In order to identify the functional roles and the interaction between mRNA and non-coding RNA (ncRNA, including lncRNA, circRNA and miRNA) in CC cisplatin (DDP) resistance, the transcription profile analysis was performed and a RNA regulatory model of CC DDP resistance was proposed. Methods In this study, whole-transcriptome sequencing analysis was conducted to study the ncRNA and mRNA profiles of parental SiHa cells and DDP resistant SiHa/DDP cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed for pathway analysis based on the selected genes with significant differences in expression. Subsequently, ceRNA network analyses were conducted using the drug resistance-related genes and signal-transduction pathways by Cytoscape software. Furthermore, a ceRNA regulatory pathway, namely lncRNA-AC010198.2/hsa-miR-34b-3p/STC2, was selected by RT-qPCR validation and literature searching. Further validation was done by both dual-luciferase reporter gene assays and RNA pull-down assays. Besides that, the changes in gene expression and biological function were further studied by performing si-AC010198.2 transfection and DDP resistance analyses in the SiHa and SiHa/DDP cells, respectively. Results Using bioinformatics and dual-luciferase reporter gene analyses, we found that AC010198.2/miR-34b-3p/STC2 may be a key pathway for DDP resistance in CC cells. Significant differences in both downstream gene expression and the biological function assays including colony formation, migration efficiency and cell apoptosis were identified in AC010198.2 knockdown cells. Conclusions Our study will not only provide new markers and potential mechanism models for CC DDP resistance, but also discover novel targets for attenuating it.

scholarly journals A Novel Circular RNA CircRFX3 Serves as a Sponge for MicroRNA-587 in Promoting Glioblastoma Progression via Regulating PDIA3

2021 ◽  
Vol 9 ◽  
Author(s):  
Tong Li ◽  
Jianguo Xu ◽  
Yi Liu
Keyword(s):  
Circular Rna ◽  
Molecular Therapy ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Competing Endogenous Rna ◽  
Luciferase Reporter Gene ◽  
Invasion And Migration ◽  
Downstream Target ◽  
Novel Target ◽  
And Migration

An increasing number of studies have indicated that circular RNAs (circRNAs) participate in the progression of numerous tumors. However, the functions of circRNAs in glioblastoma (GBM) remain largely unknown. In this study, we focused on a novel circRNA (hsa_circRFX3_003) that was spliced from RFX3, which we named circRFX3. We confirmed that the expression of circRFX3 was substantially increased in GBM cell lines and clinical GBM tissues. The results of a series of overexpression and knockdown assays indicated that circRFX3 could boost the proliferation, invasion, and migration of GBM cells. By performing dual-luciferase reporter gene and RNA pull-down assays, we verified that circRFX3 could sponge microRNA-587 (miR-587) to exercise its function as a competing endogenous RNA (ceRNA) in the development of GBM. In addition, PDIA3 was proven to be a downstream target of miR-587 and to regulate the Wnt/β-catenin pathway. In conclusion, circRFX3 could act as a cancer-promoting circRNA to boost the development of GBM and regulate the miR-587/PDIA3/β-catenin axis. This study might provide a novel target for the treatment of GBM with molecular therapy.

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