Long Non-Coding Ribonucleic Acid Forkhead Box P4-Antisense RNA 1 Targets microRNA-655-3p to Regulate the Proliferation, Transfer, and Invasion of Mammary Cancer Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 500-506
Author(s):  
Zhe Hu ◽  
Peien Wang ◽  
Beibei Miao ◽  
Haijiang Qu
Keyword(s):  
Cell Viability ◽  
Cancer Cells ◽  
Mammary Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Biological Processes ◽  
Ki 67 ◽  
Protein Levels ◽  
Mammary Cancer Cells

LncRNA FOXP4-AS1 expresses at a higher level in gastric carcinoma cells and can promote proliferation and other biological behaviors. However, the effect of FOXP4-AS1 on mammary cancer cells has not yet been elucidated. Therefore, this article explores the influence of lncRNA FOXP4-AS1 on the proliferation and other biological processes of mammary cancer MDA-MB-231 cells via its regulation of miRNA-655-3p. Firstly, nanoPCR was used to quantify the expression of FOXP4-AS1 and miRNA-655-3p in mammary cancer tissues and adjacent tissues. Compared to the adjacent tissues, the expression level of FOXP4-AS1 in mammary cancer tissue was significantly increased, while that of miRNA-655-3p was substantially reduced. Then, si-FOXP4-AS1, miRNA-655-3p mimics, si-FOXP4-AS1 + anti-miRNA-655-3p were transfected into human mammary cancer MDA-MB-231 cells. The transfection of si-FOXP4-AS1 or miRNA-655-3p mimics considerably reduced cell viability and the protein levels of Ki-67 and MMPs. The transfection of si-FOXP4-AS1 or miRNA-655-3p mimics could reduce cell migration and invasion. The dual-luciferase reporter assays revealed that FOXP4-AS1 could target miRNA-655-3p. The co-transfection of si-FOXP4-AS1 and anti-miRNA-655-3p increased cell viability, migration, and invasion; the same co-transfection also elevated the protein levels of Ki-67 and MMPs. In conclusion, this study suggests that knocking down FOXP4-AS1’s expression can reduce mammary cancer cells’ ability to proliferate and execute other biological processes by targeting the expression of miRNA-655-3p.

Sevoflurane Inhibits Growth and Metastasis of Cervical Cancer Through Up-Regulating miR-203 by Targeting Tumor Protein Translationally Controlled 1

2020 ◽  
Vol 10 (6) ◽  
pp. 874-883
Author(s):  
Li Zhang ◽  
Shiyou Wei ◽  
Zhenkai Xu ◽  
Wen Sun ◽  
Lihua Hang
Keyword(s):  
Cervical Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter System ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis ◽  
Cancer Tissues

Background: Cervical cancer is a type of malignancy with high incidence and high mortality in women all over the world. Recent findings revealed the role of sevoflurane in the inhibition of development of various cancer types. This study aimed to explore whether sevoflurane could suppress cells proliferation and metastasis through adjusting miR-203 expression in cervical cancer. Methods: The effects of sevoflurane on HeLa cell viability was assessed using CCK-8 assay. miR-203 level in Hela cells was determined by qRT-PCR. In addition, cells apoptosis, migration and invasion were evaluated using flow cytometry and transwell analysis respectively after sevoflurane treatment or miR-203 expression changes. Bioinformatics software (TargetScan) was used to predict the potential target genes for miR-203 and the prediction was validated using dual-luciferase reporter system. Results: Sevoflurane effectively inhibited cell viability, metastasis and stimulated apoptosis in cervical cancer. miR-203 demonstrated a low expression in cervical cancer tissues and cells and sevoflurane significantly up-regulated miR-203 expression in cervical cancer cells. Upregulation of miR-203 significantly suppressed cell growth and metastasis and induced apoptosis, while down-regulation of miR-203 presented the opposite effects in cervical cancer cells. In addition, the inhibitory effects of sevoflurane were eliminated by down-regulating miR-203 in cervical cancer cells. In addition, TPT1 was confirmed as a target gene for miR-203. Conclusion: Sevoflurane inhibited cervical cancer cells viability and metastasis through up-regulation of miR-203 expression by targeting TPT1.

scholarly journals CSF-1R as an inhibitor of apoptosis and promoter of proliferation, migration and invasion of canine mammary cancer cells

2013 ◽  
Vol 9 (1) ◽  
pp. 65 ◽  
Author(s):  
Magdalena Król ◽  
Kinga Majchrzak ◽  
Joanna Mucha ◽  
Agata Homa ◽  
Małgorzata Bulkowska ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Mammary Cancer ◽  
Migration And Invasion ◽  
Inhibitor Of Apoptosis ◽  
Canine Mammary Cancer ◽  
Mammary Cancer Cells

scholarly journals Melatonin decreases in vitro viability and migration of spheres derived from CF41.Mg canine mammary carcinoma cells

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Consuelo Serrano ◽  
Sofía Guzmán ◽  
Jose Ignacio Arias ◽  
Cristian Gabriel Torres
Keyword(s):  
Cell Viability ◽  
Cancer Cells ◽  
Mammary Carcinoma ◽  
Mammary Cancer ◽  
Carcinoma Cells ◽  
Canine Mammary Carcinoma ◽  
Mammary Carcinoma Cells ◽  
And Migration ◽  
Mammary Cancer Cells

Abstract Background Mammary cancer is a common disease affecting female dogs, where approximately 50% of the cases are malignant. There is a subpopulation of cancer cells with stem cell-like features within the tumour microenvironment, which can form in vitro spheres, cell structures that grow in anchor-free conditions. This cell population shows resistance to conventional antitumor treatments explaining in part the recurrence of some type of cancers. It has been previously reported that spheres derived from CF41.Mg canine mammary carcinoma cells exhibit several stemness features. Melatonin has shown antitumor effects on cancer mammary cells; nevertheless, its effects have been poorly evaluated on canine mammary cancer stem-like cells. In this regard, it has described that melatonin decreases the expression of OCT-4 in CMT-U2229 mammary cancer cells, a transcription factor that participates in the modulation of self-renewal and drug resistance in cancer stem-like cells. The aim of this study was to compare the effects of melatonin on viability and migration of canine mammary carcinoma CF41.Mg-spheres, and CF41.Mg-parental cells. CF41.Mg cells were grown in DMEM high-glucose medium containing 10% bovine foetal serum. CF41.Mg-spheres were cultured in ultra-low attachment plates with serum-free DMEM/F12 containing several growth factors. Cell viability (MTS reduction) and migration (transwell) assays were conducted in presence of melatonin (0.01, 0.1 or 1 mM). Results Melatonin decreased cell viability at 1 mM (P < 0.05), with a significant reduction in spheres compared to parental cells at 24 and 48 h (P < 0.05). Cell migration was inhibited in response to non-cytotoxic concentration of melatonin (0.1 mM) (P < 0.05) in spheres and monolayer of cells, no significant differences were detected between both cell subtypes. Conclusions These results indicate that melatonin reduces viability and migration of CF41.Mg cells, where spheres exhibit greater sensitivity to the hormone. Thus, melatonin represents a valuable potential agent against mammary cancer cells, especially cancer stem-like cells.

scholarly journals LncRNA TP73-AS1 sponges miR-141-3p to promote the migration and invasion of pancreatic cancer cells through the up-regulation of BDH2

2019 ◽  
Vol 39 (3) ◽  
Author(s):  
Xian-Ping Cui ◽  
Chuan-Xi Wang ◽  
Zhi-Yi Wang ◽  
Jian Li ◽  
Ya-Wen Tan ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Human Pancreatic Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Pancreatic Cancer Cells ◽  
Candidate Target ◽  
Direct Target

Abstract LncRNA TP73 antisense RNA 1T (TP73-AS1) plays an important role in human malignancies. However, the levels of TP73-AS1 and its functional mechanisms in pancreatic cancer metastasis remain unknown, and the clinical significance of TP73-AS1 in human pancreatic cancer is also unclear. In the present study, the levels of TP73-AS1 and its candidate target miR-141 in pancreatic cancer and adjacent normal tissue were detected using qRT-PCR. The association between TP73-AS1 levels and the clinicopathologic characteristics of pancreatic cancer patients were analyzed. The relationship between TP73-AS1 and miR-141, and miR-141 and its candidate target 3-hydroxybutyrate dehydrogenase type 2 (BDH2) was confirmed using dual-luciferase reporter assays. TP73-AS1 and/or miR-141 were knocked down using siRNA or an inhibitor in pancreatic cancer cells and cell migration and invasion then examined. The results showed that TP73-AS1 was up-regulated in pancreatic cancer tissue and cell lines. High levels of TP73-AS1 were correlated with poor clinicopathological characteristics and shorter overall survival. MiR-141 was a direct target for TP73-AS1, while BDH2 was a direct target for miR-141. The knockdown of TP73-AS1 significantly inhibited the migration and invasion of pancreatic cancer cells, while the miR-141 inhibitor significantly restored the migration and invasion. Therefore, TP73-AS1 positively regulated BDH2 expression by sponging miR-141. These findings suggest that TP73-AS1 serves as an oncogene and promotes the metastasis of pancreatic cancer. Moreover, TP73-AS1 could serve as a predictor and a potential drug biotarget for pancreatic cancer.

scholarly journals Up-regulation of miR-1825 inhibits the progression of glioblastoma by suppressing CDK14 though Wnt/β-catenin signaling pathway

2020 ◽  
Author(s):  
Fengqin Lu ◽  
Chunhong Li ◽  
Yuping Sun ◽  
Ting Jia ◽  
Na Li ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Protein Levels ◽  
Qrt Pcr ◽  
Cell Progression ◽  
Tissue Specimens

Abstract Background: Mounting evidences displayed that miRNAs play crucial roles in tumor initiation and development. However, the regulation and relevant mechanism of miR- miR-1825 in glioblastoma (GBM) remain unclear. Methods: qRT-PCR was used to detect miR-1825 and CDK14 mRNA expression. Western blot was applied for testing protein levels (VEGF, E-cadherin, N-cadherin, vimentin, β-catenin, c-myc, p-c-Jun). MTT and transwell assays were used for detecting GBM cell progression, including cell viability, migration, and invasion.Results: The results showed that miR-1825 was decreased in GBM tissue specimens by qRT-PCR and it was confirmed as a prognostic marker of GBM by Kaplan-Meier survival analysis. Moreover, we also found that miR-1825 up-regulation suppressed GBM cell viability, tumor growth, invasion and migration. Furthermore, CDK14 was first identified as the direct target of miR-1825 by Luciferase reporter assay. CDK14 acted as an oncogene in GBM development by Immunohistochemistry. In addition, Western blot analysis demonstrated that miR-1825 regulated Wnt/β-catenin signaling pathway in GBM development. Conclusion: In conclusion, miR-1825 up-regulation suppressed GBM progression by targeting CDK14 through Wnt/β-catenin pathway.

scholarly journals Aloperine prevents hypoxia-induced epithelial-mesenchymal transition in bladder cancer cells through regulating the mTOR/p70S6K/4E-BP1 pathway

2020 ◽  
Author(s):  
Weiling Lv ◽  
Qian Liu ◽  
Jihong An ◽  
Xiaoyong Song
Keyword(s):  
Bladder Cancer ◽  
Western Blot ◽  
Cell Viability ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Protein Levels ◽  
T24 Cells ◽  
Bladder Cancer Cells

Abstract Background: Aloperine (ALO), a novel active alkaloid extracted from S. alopecuroide, has been reported to possess anti-tumor effect. However, its potential effect on bladder cancer remains unknown. Therefore, the objective of this study was to investigate the effect of ALO bladder cancer cells under hypoxia condition.Methods: Human bladder cancer cell line T24 cells were treated with different concentrations of ALO and maintained in hypoxic condition for 12, 24, or 48 h. MTT assay was performed to detect cell viability. Transwell assay was performed to detect cell migration and invasion. Epithelial-mesenchymal transition (EMT) was evaluated by detecting the expression levels of E-cadherin, N-cadherin, and vimentin using western blot. The mRNA and protein levels of HIF-1α, snail, slug, and twist1 were measured using qRT-PCR and western blot. The expression levels of mTOR/p70S6K/4E-BP1 pathway-related proteins were detected using western blot.Results: Our results showed that ALO inhibited the cell viability of T24 cells cultured in hypoxia condition. ALO also attenuated hypoxia-induced migration and invasion of T24 cells. We also found that ALO treatment caused a significant increase in E-cadherin expression and decreases in N-cadherin and vimentin expressions. Besides, ALO dose-dependently inhibited the expressions of EMT inducers including snail, slug, and twist1 both in mRNA and protein levels in T24 cells induced by hypoxia. Furthermore, ALO significantly inhibited HIF-1α protein synthesis and phosphorylation of mTOR, as well 4E-BP1 and p70S6K in hypoxia-induced T24 cells.Conclusion: These results indicated that ALO exerted anti-tumor effect on bladder cancer in vitro via inhibiting the activation of mTOR/p70S6K/4E-BP1 pathway.

scholarly journals Berberine Inhibits the Expression of SCT through miR-214-3p Stimulation in Breast Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Congyuan Zhu ◽  
Jianping Li ◽  
Yuming Hua ◽  
Jingli Wang ◽  
Ke Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Transwell Invasion Assay ◽  
Underlying Mechanisms ◽  
Mcf 7

In this study, we aimed to evaluate the suppressive abilities of berberine (BBR) on MCF-7 and MDA-MB-231 cells and confirm its underlying mechanisms on miR-214-3p. We first built a panel of 18 miRNAs and 9 lncRNAs that were reported to participate in the mechanism of breast cancer. The RT-qPCR results suggested that BBR illustrated a dosage-dependent pattern in the stimulation to miR-214-3p in both MCF-7 and MDA-MB-231 cells. Then, we performed gain-and-lose function tests to validate the role of miR-214-3p contributing to the anticancer effects of BBR. Both BBR and miR-214-3p mimic reduced the cell viability, repressed migration and invasion capacities, increased rates of total apoptotic cells and ratio of Bax/Bcl-2, and increased the percentage of G2/M cells of MCF-7 and MDA-MB-231 cells by colony formation and CKK8 assay, scratch wound healing and gelatin-based 3D conformation assay, transwell invasion assay, and cell cycle analysis, respectively. However, miR-214-3p inhibitor counteracted all these effects of BBR. Based on the bioinformatics analysis and dual-luciferase reporter test, we identified binding sites between SCT and miR-214-3p. We further confirmed that BBR massively and dose-dependently reduced the mRNA expression and protein levels of SCT in both MCF-7 and MDA-231 cells. We testified that both miR-214-3p mimic and BBR could decrease the mRNA expression and protein levels of SCT, while miR-214-3p inhibitor weakened these reductions. In conclusion, BBR suppressed MCF-7 and MDA-MB-231 breast cancer cells by upregulating miR-214-3p and increasing its inhibition to SCT.

Research on the Negatively Regulation of Long Intergenic Non-Coding RNA 00210 to miR-424-5p in Breast Cancer Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 520-526
Author(s):  
Xingguo Cui ◽  
Weiguang Xu
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Cell Behaviors ◽  
Non Coding Rna ◽  
Set Up ◽  
E Cadherin

In this work, we investigate the expression of long intergenic non-coding RNA 00210 (LINC00210) and its effects on the behavior of breast cancer cells. To this end, we measured LINC00210 and miR-424-5p expression using RT-qPCR. Bioinformatics, dual luciferase report experiments, and RT-qPCR were applied to determine the potential function of LINC00210 in the regulation of miR-424-5p. Four groups of T-47D cells were set up: si-NC, si-LINC00210, si-LINC00210 + anti-miR-NC, and si-LINC00210 + anti-miR-424-5p. Then, cell viability, apoptosis, migration, and invasion were detected, respectively. Western blot analysis was applied to measure the expression levels of E-cadherin, N-cadherin, Bax, and Bcl-2. Our results showed that breast cancer tissue highly expressed LINC00210 and slightly expressed miR-424-5p, and that a direct binding function of LINC00210 to miR-424-5p existed. Furthermore, many of the behaviors of T-47D cells in the si-LINC00210 group were affected, including reductions in cell viability, migration and invasion abilities, as well as decreased expressions of LINC00210, Ki67, Bcl-2, and N-cadherin, an increased apoptosis rate, and increased expressions of miR-424-5p, E-cadherin, and Bax. In addition, in comparison with the si-LINC00210 + anti-miR-NC group, the cell behaviors of T-47D cells in the si-LINC00210 + anti-miR-424-5p group were affected, including increased cell viability, migration and invasion abilities, and expressions of Ki67, Bcl-2, and N-cadherin, but reductions in E-cadherin and Bax. The results demonstrated the inhibitory effects of LINC00210 on T-47D cells, as well as the negative regulation of LINC00210 on miR-424-5p, leading to cell apoptosis. The results imply the potential value of LINC00210 as a therapeutic target for breast cancer.

scholarly journals Circular RNA circ-MMP11 Contributes to Lapatinib Resistance of Breast Cancer Cells by Regulating the miR-153-3p/ANLN Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaoli Wu ◽  
Yi Ren ◽  
Rong Yao ◽  
Leilei Zhou ◽  
Ruihua Fan
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Migration And Invasion

BackgroundDrug-resistance is a major obstacle to the treatment of breast cancer. Circular RNA (circRNA) circ-MMP11 has been reported to be promoting the progression of breast cancer. This study is designed to explore the role and mechanism of circ-MMP11 in lapatinib resistance in breast cancer.MethodsCirc-MMP11, microRNA-153-3p (miR-153-3p), and Anillin (ANLN) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, number of colonies, apoptosis, migration, and invasion were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, flow cytometry, and transwell assays, respectively. Exosomes were exerted and detected by differential centrifugation and a transmission electron microscope. The protein levels of CD63, CD9, and ANLN were assessed by western blot assay. The binding relationship between miR-153-3p and circ-MMP11 or ANLN was predicted by circinteractome or starbase, and then verified by a dual-luciferase reporter assay and RNA pull-down assay. The biological role of circ-MMP11 on breast cancer tumor growth and drug resistance was detected by the xenograft tumor model in vivo.ResultsCirc-MMP11 and ANLN were highly expressed, and miR-153-3p was decreased in LR breast cancer tissues and cells. Circ-MMP11 could be transported by exosomes. Furthermore, circ-MMP11 knockdown promoted lapatinib sensitivity by repressing cell viability, colony number, migration, invasion, and boosting apoptosis in LR breast cancer cells. Circ-MMP11 deficiency improved the drug sensitivity of breast cancer in vivo. Mechanically, circ-MMP11 could regulate ANLN expression through sponging miR-153-3p.ConclusionCirc-MMP11 could be transferred by exosomes in breast cancer cells. And circ-MMP11 functioned as a sponge of miR-153-3p to regulate ANLN expression, thereby promoting lapatinib resistance in breast cancer cells, providing therapeutic targets for the treatment of breast cancer.

scholarly journals MicroRNA-96-5p Facilitates the Viability, Migration, and Invasion and Suppresses the Apoptosis of Cervical Cancer Cells byNegatively Modulating SFRP4

2020 ◽  
Vol 19 ◽  
pp. 153303382093413 ◽  
Author(s):  
Huiling Zhang ◽  
Ruxin Chen ◽  
Jinyan Shao
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Clinical Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Related Protein ◽  
Siha Cells ◽  
Gene Assay ◽  
Cervical Cancer Cells ◽  
Cancer Tissues

Purpose: The current study was intended to research the functional role and regulatory mechanism of microRNA-96-5p in the progression of cervical cancer. Methods: MicroRNA-96-5p expression in cervical cancer tissues was assessed by quantitative real-time polymerase chain reaction. The association between microRNA-96-5p expression and clinicopathological features of patients with cervical cancer was analyzed. MTT, flow cytometry, wound healing, and transwell assay were performed to evaluate the viability, apoptosis, migration, and invasion of Hela and SiHa cells. Targetscan, dual-luciferase reporter gene assay, and RNA pull-down analysis were constructed to evaluate the target relationship between microRNA-96-5p and secreted frizzled-related protein 4. Results: MicroRNA-96-5p was overexpressed in cervical cancer tissues, and microRNA-96-5p expression was markedly associated with the clinical stage and lymph node metastasis of patients with cervical cancer. Overexpressed microRNA-96-5p facilitated the viability, migration, invasion, and inhibited the apoptosis of Hela and SiHa cells, whereas suppression of microRNA-96-5p exerted the opposite trend. Secreted frizzled-related protein 4 was proved to be a target of microRNA-96-5p. Silencing of secreted frizzled-related protein 4 eliminated the anti-tumor effect of microRNA-96-5p on cervical cancer cells. Conclusions: MicroRNA-96-5p facilitated the viability, migration, and invasion and inhibited the apoptosis of cervical cancer cells via negatively regulating secreted frizzled-related protein 4.

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