miR-146a promoted breast cancer proliferation and invasion by regulating NM23-H1

2019 ◽  
Vol 167 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Jun Chen ◽  
Qiang Jiang ◽  
Xue-Qin Jiang ◽  
De-Quan Li ◽  
Xiao-Cheng Jiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell Line ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Regulatory Relationship ◽  
Cancer Proliferation ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Proliferation And Invasion

Abstract The study aimed to investigate the regulatory effect of miR-146a in proliferation, invasion and migration of breast cancer and its possible mechanism via NM23-H1. The expression levels of miR-146a in breast cancer with different pathological classification were significantly increased, while the expression levels of NM23-H1 were significantly decreased, which were closely correlated. Double luciferase reporter gene was used to verify the target regulatory relationship between miR-146 and NM23-H1 on a human breast cancer cell line. miR-146a was closely related to the proliferation and metastasis of breast cancer. miR-146a also promoted the growth of breast cancer in vivo via targeting NM23-H1. In conclusion, miR-146 can promote the proliferation and invasion of breast cancer by targeting NM23-H1.

Knockdown of LncRNA-UCA1 Inhibits Breast Cancer Growth in Association with METTL14/miR-375/SOX12 Axis

2020 ◽  
Author(s):  
Chengpeng Zhao ◽  
Xiaoling Ling ◽  
Yunxia Xia ◽  
Bingxue Yan ◽  
Quanlin Guan
Keyword(s):  
Breast Cancer ◽  
Dna Methyltransferase ◽  
Dna Methyltransferases ◽  
Cancer Prognosis ◽  
Luciferase Reporter ◽  
Cancer Growth ◽  
Western Blots ◽  
Breast Cancer Growth ◽  
Proliferation And Invasion

Abstract Background Breast cancer is a malignant tumor with high incidence in females. Burgeoning studies have analyzed the relationship between long non-coding RNA (lncRNA) and breast cancer. However, the role of LncRNA UAC1 in the pathogenesis of breast cancer remains unclear. Methods LncRNA-UCA1 levels were detected in breast cancer tissues and cells while correlation between LncRNA-UCA1 expression and patient survival was analyzed by the Kaplan-Meier. The proliferation, invasion and apoptosis of cells were measured by CCK-8 assay, Transwell test and flow cytometry, respectively. Protein levels of apoptosis-related factors were assessed by Western blots. RIP test detected the combination of LncRNA-UCA1 and DNA methyltransferases whereas RNA pull-down test showed the interaction of DNA methyltransferases and LncRNA UCA1. Enrichment of DNA transferase of METTL14 promoter in T47D was assessed by ChIP. Interaction between miR-375 and SOX12 was confirmed via dual-luciferase reporter assay. Tumorigenesis was observed in vivo. Results LncRNA-UCA1 levels were increased in breast cancer and a high LncRNA-UCA1 level was a risk factor of the poor breast cancer prognosis. Silencing LncRNA-UCA1 inhibited the proliferation and invasion but promoted apoptosis of breast cancer cells. LncRNA-UCA1 recruited DNA methyltransferase to the METTL14 promoter region to inhibit METTL14 expression in breast cancer. Low METTL14 levels were associated with stronger proliferation and invasion abilities, whereas weaker proliferation and invasion abilities were related to low LncRNA-UCA1 levels. METTL14 mediated the low expression of miR-375 by m6A modification in breast cancer. Conclusion Depleted LncRNA-UCA1 inhibited breast cancer growth by regulating the METTL14-miR-375-SOX12 axis in vitro and in vivo.

scholarly journals NcRNAs-mediated High Expression of TIMM8A Correlates with Poor Prognosis and Act as an Oncogene in Breast Cancer

2021 ◽  
Author(s):  
Zhonglin Wang ◽  
Shuqin Li ◽  
Feng Xu ◽  
Jingyue Fu ◽  
Jie Sun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Poor Prognosis ◽  
Molecular Mechanisms ◽  
Human Cancer ◽  
Luciferase Reporter ◽  
Inner Mitochondrial Membrane ◽  
Cancer Proliferation ◽  
Bioinformatics Analyses

Abstract Background: Breast cancer is notorious for its increasing incidence for decades. Ascending evidence has demonstrated that translocase of inner mitochondrial membrane (TIMM) proteins play vital roles in progression of several types of human cancer. However, the biological behaviors and molecular mechanisms of TIMM8A in breast cancer remain not fully illustrated.Methods: Pan-cancer analysis was firstly performed for TIMM8A’s expression and prognosis by Oncomine database. Subsequently, TIMM8A-related noncoding RNAs (ncRNAs) were identified by a series of bioinformatics analyses and dual-luciferase reporter assay, including expression analysis, correlation analysis, and survival analysis. Moreover, the effect of TIMM8A on breast cancer proliferation and apoptosis was evaluated in vitro by CCK-8 assays, colony formation assays and Western blot assays and the in vivo effect was revealed through a patient-derived xenograft mouse model.Results: We found that TIMM8A showed higher expression level in breast cancer and the higher TIMM8A mRNA expression group had a poorer prognosis than the lower TIMM8A group. hsa-circ-0107314/hsa-circ-0021867/hsa-circ-0122013 might be the three most potential upstream circRNAs of hsa-miR-34c-5p/hsa-miR-449a-TIMM8A axis in breast cancer. TIMM8A promotes proliferation of breast cancer cells in vitro and tumor growth in vivo.Conclusion: Our results confirmed that ncRNAs-mediated upregulation of TIMM8A correlated with poor prognosis and act as an oncogene in breast cancer.

scholarly journals Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1

2020 ◽  
Vol 25 (1) ◽  
Author(s):  
Minhao Lv ◽  
Qixin Mao ◽  
Juntao Li ◽  
Jianghua Qiao ◽  
Xiuchun Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Quantitative Polymerase Chain Reaction ◽  
Polymerase Chain Reaction Analysis ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Coding ◽  
Expression Levels ◽  
Reporter Assays ◽  
Proliferation And Invasion

Abstract Background Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown. Methods LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis. Results LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p. Conclusion LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.

scholarly journals DSCAM-AS1 promotes tumor growth of breast cancer by reducing miR-204-5p and upregulatingRRM2

2018 ◽  
Author(s):  
Wen-Hui Liang ◽  
Na Li ◽  
Zhi-Qing Yuan ◽  
Xin-Lai Qian ◽  
Zhi-Hui Wang
Keyword(s):  
Breast Cancer ◽  
Microarray Analysis ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Cell Transfection ◽  
Transwell Assay ◽  
Qrt Pcr ◽  
Summary Statement ◽  
Proliferation And Invasion

AbstractWe intended to analyze the effects of DSCAM-AS1, miR-204-5p andRRM2on breast cancer (BC) cells growth. Microarray analysis and qRT-PCR were employed to determine DSCAM-AS1 and miR-204-5p expression in BC. Luciferase reporter assay and cell transfection assay were applied to examine the target relationship between DSCAM-AS1, miR-204-5p and MMR2. CCK-8 assay, transwell assay and flow cytometry were used to detect cell proliferation, invasion and apoptosis of breast cancer cells. The expression of DSCAM-AS1, miR-204-5p and MMR2 were confirmed by Western Blot. We also conductedIn vivoassay to verify the effect of DSCAM-AS1 on tumor formation.DSCAM-AS1 was up-regulated, while miR-204-5p was down-regulated in BC tissues and cells. Meanwhile, DSCAM-AS1 directly targeted miR-204-5p. DSCAM-AS1 promoted the proliferation and invasion of BC cells and restrained cell apoptosis by reducing miR-204-5p and inhibiting miR-204-5p expression.RRM2was up-regulated in BC cells, and miR-204-5p inhibitedRRM2expression by targetingRRM2. Overexpression ofRRM2stimulated proliferation and cell invasion and impeded apoptosis of BC cells.In vivoexperiments showed that knockdown of DSCAM-AS1 decreased the tumorigenesis of BC cells, increased the expression of miR-204-5p while inhibitedRRM2expression.DSCAM-AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR-204-5p and enhancingRRM2expression. DSCAM-AS1/miR-204-5p/RRM2may serve as novel therapeutic targets for BC.Summary statementMicroarray analysis and qRT-PCR were employed to determine DSCAM-AS1 and miR-204-5p expression in BC. DSCAM-AS1 promoted proliferation and impaired apoptosis of BC cells by reducing miR-204-5p and enhancingRRM2expression.

scholarly journals miR-185 Inhibits the Proliferation and Invasion of Non-Small Cell Lung Cancer by Targeting KLF7

2019 ◽  
Vol 27 (9) ◽  
pp. 1015-1023 ◽  
Author(s):  
Lili Zhao ◽  
Yao Zhang ◽  
Jiaoxia Liu ◽  
Wei Yin ◽  
Dan Jin ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Mesenchymal Transition ◽  
Normal Tissues ◽  
Cancer Types ◽  
Proliferation And Invasion

MicroRNAs (miRNAs) are short endogenous noncoding RNAs that frequently play vital roles in many cancer types. Herein we demonstrated that miR-185 was remarkably downregulated in NSCLC tissues compared with adjacent normal tissues. A lower level of miR-185 was associated with lymph node metastasis. Functional assays showed that upregulation of miR-185 inhibited the proliferation, colony formation, and invasion capacities of NSCLC cells in vitro. Furthermore, we found that miR-185 suppressed the epithelial‐mesenchymal transition (EMT) process. Bioinformatics analysis and luciferase reporter gene assays revealed that Kruppel-like factor 7 (KLF7) was the target of miR-185. Overexpression of miR-185 reduced the expression of KLF7 in NSCLC cells. Upregulation of KLF7 partly neutralized the inhibitory effects of miR-185 on the proliferation and invasion of NSCLC. Additionally, we confirmed that miR-185 suppressed the tumor growth of NSCLC A549 cells in vivo. Taken together, these results demonstrate that miR-185 acts as a suppressor by targeting KLF7 in NSCLC.

scholarly journals Silencing of FTX suppresses pancreatic cancer cell proliferation and invasion by upregulating miR-513b-5p

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shan Li ◽  
Qian Zhang ◽  
Wen Liu ◽  
Chunbo Zhao
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Migration Ability ◽  
Expression Levels ◽  
Gene Assay ◽  
Competitive Endogenous Rna

Abstract Background Abnormal expression of long non-coding RNA (lncRNA) FTX (five prime to Xist), which is involved in X chromosome inactivation, has been reported in various tumors. However, the effect of FTX on the development of pancreatic cancer (PC) has not been elucidated. The purpose of this study was to explore the possible molecular mechanism of FTX in PC. Methods Quantitative real-time PCR (qRT-PCR) was used to measure the expression levels of FTX and miR-513b-5p in PC cell lines. Proliferation and apoptosis of PC cells were determined by CCK-8, Edu assay, and flow cytometry. Invasion and migration ability of PC cells were detected by Transwell assay and scratch test. Bioinformatics analysis, luciferase reporter gene assay, and RNA immunoprecipitation (RIP) assay were used to verify the direct binding between FTX and miR-513b-5p. The xenotransplantation mouse model was established to explore the effect of FTX and miR-513b-5p on the PC tumor growth in vivo. Results The expression levels of FTX were increased in PC cell lines, and silencing of FTX remarkably suppressed the invasion ability and cell viability. Besides, FTX could bind to miR-513b-5p as a competitive endogenous RNA, thus promoting the invasion and proliferation ability of PC cells. Moreover, knockdown of FTX inhibited the tumor growth and increased the expression levels of miR-513b-5p and apoptosis-related proteins in vivo. Conclusions FTX could directly combine with miR-513b-5p as a competitive endogenous RNA, thus promoting the occurrence and development of PC in vitro and in vivo.

Long non-coding RNA HCG18 promotes malignant phenotypes of breast cancer (BC) cells by HCG18/miR-103a-3p/UBE2O/mTORC1/HIF-1α positive feedback loop

2021 ◽  
Author(s):  
Xu Liu ◽  
Kun Qiao ◽  
Kaiyuan Zhu ◽  
Xianglan Li ◽  
Chunbo Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Bioinformatic Analysis ◽  
In Vitro Assays ◽  
Luciferase Reporter ◽  
Regulatory Relationship ◽  
Positive Feedback Loop

Abstract Background: In recent years, a growing number of studies have reported that long non-coding RNAs (LncRNAs) play crucial roles in breast cancer (BC) progression and metastasis. Another study group of our research center reported that LncRNA HCG18 was one of the 30 upregulated lncRNAs in BC tissues related to normal tissues in TCGA database. However, the exactly biological roles of HCG18 in BC remains unclear. Method: qRT-PCR was used to detect the expression profile of HCG18 in BC tissues and cell lines. In vitro assays were used to evaluate the pro-tumor function of HCG18 in BC cells. Animal study were used to explore the role of HCG18 in vivo. Bioinformatic analysis, dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and Chromatin Immunoprecipitation (ChIP) assays were used to investigate the regulatory relationship of HCG18, miR-103a-3p, UBE2O in BC. Results: HCG18 was upregulated in BC tissues and cells, and BC patients with high HCG18 expression tended to have poor prognosis. HCG18 could promote BC cells proliferation, invasion and provided BC cells with tumor stemness properties (CSPs) in vitro and facilitate tumor growth and lung metastasis in vivo. In terms of mechanism, HCG18 functioned as a miRNA sponge which positively regulated the expression of Ubiquitin-conjugating enzyme E2O (UBE2O) by sponging miR-103a-3p and our previous research achievement have already verified UBE2O could promote malignant phenotypes of BC cells through UBE2O/AMPKα2/mTORC1 axis. Furthermore, as a downstream target of HCG18/miR-103a-3p/UBE2O/mTORC1 axis, HIF-1α transcriptionally promoted HCG18 expression and then formed a positive feedback loop in BC. Conclusion: HCG18 played an oncogenic role in BC and it might serve as a prognostic biomarker and a potential therapeutic target for BC treatment.

scholarly journals miR-224-5p Carried by Human Umbilical Cord Mesenchymal Stem Cells-Derived Exosomes Regulates Autophagy in Breast Cancer Cells via HOXA5

2021 ◽  
Vol 9 ◽  
Author(s):  
Yichao Wang ◽  
Pan Wang ◽  
Lei Zhao ◽  
Xiaoying Chen ◽  
Zhu Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Rna Binding ◽  
Luciferase Reporter ◽  
Human Umbilical Cord ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Objective: In this study, we focused on the potential mechanism of miRNAs carried by human umbilical cord mesenchymal stem cells-derived exosomes (hUCMSCs-exo) in breast cancer (BC).Methods: RT-qPCR was conducted for the expression of miR-224-5p and HOXA5 in tissues and cells. After co-culture of exosomes and MCF-7 or MDA-MB-231 cells, the cell proliferation was observed by MTT and cell colony formation assay, while apoptosis was measured by flow cytometry. In addition, the expression of HOXA5 and autophagy pathway-related proteins LC3-II, Beclin-1 and P62 was detected by western blotting. And immunofluorescence was applied for detection of LC3 spots. The binding of miR-224-5p to HOXA5 was verified by the luciferase reporter gene assay and RNA-binding protein immunoprecipitation assay. Finally, in vivo experiment was performed to investigate the effect of miR-224-5p on BC growth.Results: MiR-224-5p was up-regulated and HOXA5 was down-regulated in BC tissues and cells. HOXA5 was confirmed to be the target gene of miR-224-5p. MiR-224-5p carried by hUCMSCs-exo was able to promote the proliferation and autophagy of BC cells, while inhibited apoptosis. Bases on xenograft models in nude mice, it was also revealed that miR-224-5p carried by hUCMSCs-exo could regulate autophagy and contribute to the occurrence and development of BC in vivo.Conclusion: MiR-224-5p carried by hUCMSCs-exo can regulate autophagy via inhibition of HOXA5, thus affecting the proliferation and apoptosis of BC cells.

scholarly journals Linc00460/miR-641 promoted promotes proliferation and autophagy of breast cancer

2020 ◽  
Author(s):  
Wei Zhang ◽  
Huimin Zhang ◽  
Bin Wang ◽  
Yu Ren ◽  
Jianjun He ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Luciferase Reporter ◽  
In Vitro Tests ◽  
Luciferase Reporter Gene ◽  
Qrt Pcr ◽  
In Vivo Tests ◽  
Worse Prognosis

Abstract This manuscript aimed to investigate the oncogenic role of linc00460 in breast cancer both in vivo and in vitro and then specify its downstream microRNAs to build a ceRNA network. As for in vivo tests, we used subgroup analysis and nomogram for survival analysis. As for in vitro tests, qRT-PCR, CCK-8 and Dual luciferase reporter gene were used. Linc00460 expressed highly in breast cancer. The nomogram indicated that linc00460 was associated with worse prognosis. Linc00460 might negatively regulate miR-641 to promote the proliferation and autophagy of breast cancer cell. In conclusion, linc00460 could be a risk factor for breast cancer by regulating miR-641; and it has the potential to be a novel biomarker.

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