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  5. How Does Doi.org Make Money
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We began analyzing https://www.nature.com/articles/s41419-019-1705-z, but it redirected us to https://www.nature.com/articles/s41419-019-1705-z. The analysis below is for the second page.

Title[redir]:
miR-665 expression predicts poor survival and promotes tumor metastasis by targeting NR4A3 in breast cancer | Cell Death & Disease
Description:
Cancer metastasis is the main cause of death in breast cancer (BC) patients. Therefore, prediction and treatment of metastasis is critical for enhancing the survival of BC patients. In this study, we aimed to identify biomarkers that can predict metastasis of BC and elucidate the underlying mechanism of the functional involvement of such markers in metastasis. miRNA expression profile was analyzed using a custom microarray system in 422 BC tissues. The relationship between the upregulated miR-665, metastasis and survival of BC was analyzed and verified in another set of 161 BC samples. The biological function of miR-665 in BC carcinogenesis was explored with in vitro and in vivo methods. The target gene of miR-665 and its signaling cascade were also analyzed. There are 399 differentially expressed miRNAs between BC and noncancerous tissues, of which miR-665 is the most upregulated miRNA in the BC tissues compared with non-tumor breast tissues (P < 0.001). The expression of miR-665 predicts metastasis and poor survival in 422 BC patients, which is verified in another 161 BC patients and 2323 BC cases from online databases. Ectopic miR-665 expression promotes epithelial–mesenchymal transition (EMT), proliferation, migration and invasion of BC cells, and increases tumor growth and metastasis of BC in mice. Bioinformatics, luciferase assay and other methods showed that nuclear receptor subfamily 4 group A member 3 (NR4A3) is a target of miR-665 in BC. Mechanistically, we demonstrated that miR-665 promotes EMT, invasion and metastasis of BC via inhibiting NR4A3 to activate MAPK/ERK kinase (MEK) signaling pathway. Our study demonstrates that miR-665 upregulation is associated with metastasis and poor survival in BC patients, and mechanistically, miR-665 enhances progression of BC via NR4A3/MEK signaling pathway. This study provides a new potential prognostic biomarker and therapeutic target for BC patients.

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 96,105,781 visitors per month in the current month.

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The income method remains a mystery to us.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Doi.org has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

cells, nra, expression, cancer, cell, metastasis, article, patients, fig, breast, control, google, scholar, compared, tumor, mdamb, tissues, mcf, assay, survival, analysis, invasion, cas, emt, inhibitor, promotes, migration, significantly, results, mice, china, showed, mimics, mrna, protein, levels, mirna, target, luciferase, increased, gene, lung, βcatenin, poor, mek, usa, result, samples, signaling, growth,

Topics {✒️}

nature portfolio bio-rad mini-trans-blot apparatus privacy policy china/joint research fund nature advertising sun yat-sen university lv-mir-control-zr-75-30 cells separately goat anti-rabbit igg mixed solutions social media lv-mir-665-zr-75-30 cells magnification real-time rt-pcr analysis previous research kaplan–meier plotter database reprints kapla–meier plotter database mir-665/tgfbr1-tgfbr2/smad2/3 pathway tgf-betarii predicts bone lv-mir-control-zr-75-30 cells lv-mir-control-zr-70-30 cells research lv-mir-nc-zr-75-30 cells hybrid epithelial/mesenchymal phenotype annexin v-fluorescein isothiocyanate full size image aberrant jak/stat signaling quantitative real-time pcr pre-menopausal breast cancer phenol/chloroform extraction method activate mapk/erk kinase dual-reporter system consisting hui-yun wang dual-luciferase reporter assay mir-665-expressing cells died nr4a3-silenced mda-mb-231 cells 1 × 107 lv-mir-665-zr-75-30 cells lv-mir-665-zr-75-30 cells lv-mir-665-zr-70-30 cells lv-mir-control-zr-75-30 extracellular signal-regulated kinase ewsr1-nr4a3 gene fusion promotes tgfbeta-induced metastasis early-stage breast cancer permissions quantitative rt-pcr showed nr4a3/mek signaling pathway disease-free survival low-input total rna kaplan–meier estimator

Questions {❓}

  • OncomiR or tumor suppressor?

Schema {🗺️}

WebPage:
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         headline:miR-665 expression predicts poor survival and promotes tumor metastasis by targeting NR4A3 in breast cancer
         description:Cancer metastasis is the main cause of death in breast cancer (BC) patients. Therefore, prediction and treatment of metastasis is critical for enhancing the survival of BC patients. In this study, we aimed to identify biomarkers that can predict metastasis of BC and elucidate the underlying mechanism of the functional involvement of such markers in metastasis. miRNA expression profile was analyzed using a custom microarray system in 422 BC tissues. The relationship between the upregulated miR-665, metastasis and survival of BC was analyzed and verified in another set of 161 BC samples. The biological function of miR-665 in BC carcinogenesis was explored with in vitro and in vivo methods. The target gene of miR-665 and its signaling cascade were also analyzed. There are 399 differentially expressed miRNAs between BC and noncancerous tissues, of which miR-665 is the most upregulated miRNA in the BC tissues compared with non-tumor breast tissues (P < 0.001). The expression of miR-665 predicts metastasis and poor survival in 422 BC patients, which is verified in another 161 BC patients and 2323 BC cases from online databases. Ectopic miR-665 expression promotes epithelial–mesenchymal transition (EMT), proliferation, migration and invasion of BC cells, and increases tumor growth and metastasis of BC in mice. Bioinformatics, luciferase assay and other methods showed that nuclear receptor subfamily 4 group A member 3 (NR4A3) is a target of miR-665 in BC. Mechanistically, we demonstrated that miR-665 promotes EMT, invasion and metastasis of BC via inhibiting NR4A3 to activate MAPK/ERK kinase (MEK) signaling pathway. Our study demonstrates that miR-665 upregulation is associated with metastasis and poor survival in BC patients, and mechanistically, miR-665 enhances progression of BC via NR4A3/MEK signaling pathway. This study provides a new potential prognostic biomarker and therapeutic target for BC patients.
         datePublished:2019-06-17T00:00:00Z
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      headline:miR-665 expression predicts poor survival and promotes tumor metastasis by targeting NR4A3 in breast cancer
      description:Cancer metastasis is the main cause of death in breast cancer (BC) patients. Therefore, prediction and treatment of metastasis is critical for enhancing the survival of BC patients. In this study, we aimed to identify biomarkers that can predict metastasis of BC and elucidate the underlying mechanism of the functional involvement of such markers in metastasis. miRNA expression profile was analyzed using a custom microarray system in 422 BC tissues. The relationship between the upregulated miR-665, metastasis and survival of BC was analyzed and verified in another set of 161 BC samples. The biological function of miR-665 in BC carcinogenesis was explored with in vitro and in vivo methods. The target gene of miR-665 and its signaling cascade were also analyzed. There are 399 differentially expressed miRNAs between BC and noncancerous tissues, of which miR-665 is the most upregulated miRNA in the BC tissues compared with non-tumor breast tissues (P < 0.001). The expression of miR-665 predicts metastasis and poor survival in 422 BC patients, which is verified in another 161 BC patients and 2323 BC cases from online databases. Ectopic miR-665 expression promotes epithelial–mesenchymal transition (EMT), proliferation, migration and invasion of BC cells, and increases tumor growth and metastasis of BC in mice. Bioinformatics, luciferase assay and other methods showed that nuclear receptor subfamily 4 group A member 3 (NR4A3) is a target of miR-665 in BC. Mechanistically, we demonstrated that miR-665 promotes EMT, invasion and metastasis of BC via inhibiting NR4A3 to activate MAPK/ERK kinase (MEK) signaling pathway. Our study demonstrates that miR-665 upregulation is associated with metastasis and poor survival in BC patients, and mechanistically, miR-665 enhances progression of BC via NR4A3/MEK signaling pathway. This study provides a new potential prognostic biomarker and therapeutic target for BC patients.
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      dateModified:2019-06-17T00:00:00Z
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         Prognostic markers
         Translational research
         Life Sciences
         general
         Biochemistry
         Cell Biology
         Immunology
         Cell Culture
         Antibodies
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               type:PostalAddress
            type:Organization
      name:Shi-Juan Mai
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Nuo-Qing Weng
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Rui-Qi Wang
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Ji Liu
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Hui-Zhong Zhang
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:Department of Breast Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Jie-Hua He
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:Department of Breast Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Hui-Yun Wang
      affiliation:
            name:Sun Yat-Sen University Cancer Center
            address:
               name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:Department of Basic Medicine, Guiyang College of Traditional Chinese Medicine, Guiyang, China
      name:Department of Breast Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:Department of Radiation Oncology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:Department of Breast Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:Department of Breast Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China
      name:State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China

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