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We are analyzing https://link.springer.com/article/10.1007/s11596-014-1367-0.

Title:
Effects of estrogen-related receptor alpha (ERRα) on proliferation and metastasis of human lung cancer A549 cells | Current Medical Science
Description:
Estrogen-related receptor alpha (ERRα) plays an important role in the development of hormone-dependent cancers, but its roles in lung cancer remain elusive. The present study was aimed to investigate the effects of ERRα on the proliferation and metastasis of lung cancer A549 cells. The mRNA and protein levels of ERRα were detected in lung cancer A549 and MCF-7 cells and bronchial epithelial BEAS-2B cells by qRT-PCR and Western blotting, respectively. ERRα plasmid transfection and XCT-790 (an inverse agonist of ERRα) were used to up-regulate or down-regulate ERRα expression in A549 cells, respectively. The viability of A549 cells was measured by cell counting kit-8 (CCK-8) and the motility of A549 cells by wound healing assay and Transwell migration/invasion assay. The epithelial markers E-cadherin (E-Cad) and zona occludin-1 (ZO-1), the mesenchymal markers fibronectin (FN) and vimentin (Vim) and the transcription factors (Snail, Zeb1 Twist and Slug) were further detected at mRNA and protein levels by qRT-PCR and Western blotting, respectively. The results showed that ERRα promoted the growth of lung cancer A549 cells in vitro. XCT-790 significantly inhibited the migration and invasion of A549 cells. Over-expression of ERRα promoted the epithelial-to-mesenchymal transition (EMT) of A549 cells, down-regulated the epithelial makers E-Cad and ZO-1, and up-regulated the mesenchymal makers FN and Vim. Silencing of Slug, but not other transcription factors, significantly abolished the ERRα-induced EMT of A549 cells. It was suggested that ERRα promoted the migration and invasion of A549 cells by inducing EMT, and Slug was involved in the process. Targeting ERRα might be an efficient approach for lung cancer treatment.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {šŸ’ø}

We don’t know how the website earns money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {šŸ”}

article, pubmed, cancer, google, scholar, cas, receptor, cells, estrogenrelated, cell, alpha, lung, errα, expression, human, mol, cancers, access, breast, biol, central, estrogen, privacy, cookies, content, journal, proliferation, growth, migration, receptors, erralpha, information, publish, research, search, effects, metastasis, huang, yin, epithelial, xct, slug, transition, steroid, nuclear, res, data, log, huazhong, university,

Topics {āœ’ļø}

estrogen-related receptor alpha month download article/chapter estrogen receptor-related receptors epithelial markers e-cadherin estrogen-related receptor epithelial makers e-cad inverse agonist oncogenic k-ras-expressing transwell migration/invasion assay erbb2/her2 signaling pathway lung cancer a549 xct-790 significantly inhibited full article pdf authors contributed equally cell growth differ lung cancer treatment epithelial-mesenchymal transitions human breast carcinoma nat rev cancer steroid hormone receptors mol cell biol privacy choices/manage cookies fundamental research funds human breast cancer related subjects mol cell endocrinol oestrogen receptors sufficient physical activity metabolic regulator erralpha colon cancer cells cell counting kit-8 stem cell properties human prostatic cells ovarian cancer cells hormone-dependent cancers article huang epithelial-mesenchymal transition check access instant access endocr-relat cancer wound healing assay her2/igf-1r mol cancer res central universities article journal european economic area fan-na liu qi-yi zheng fo-lan li ying-xue zhong

Questions {ā“}

  • Snail, ZEB and bHLH factors in tumour progression: an alliance against the epithelial phenotype?

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:Effects of estrogen-related receptor alpha (ERRα) on proliferation and metastasis of human lung cancer A549 cells
         description:Estrogen-related receptor alpha (ERRα) plays an important role in the development of hormone-dependent cancers, but its roles in lung cancer remain elusive. The present study was aimed to investigate the effects of ERRα on the proliferation and metastasis of lung cancer A549 cells. The mRNA and protein levels of ERRα were detected in lung cancer A549 and MCF-7 cells and bronchial epithelial BEAS-2B cells by qRT-PCR and Western blotting, respectively. ERRα plasmid transfection and XCT-790 (an inverse agonist of ERRα) were used to up-regulate or down-regulate ERRα expression in A549 cells, respectively. The viability of A549 cells was measured by cell counting kit-8 (CCK-8) and the motility of A549 cells by wound healing assay and Transwell migration/invasion assay. The epithelial markers E-cadherin (E-Cad) and zona occludin-1 (ZO-1), the mesenchymal markers fibronectin (FN) and vimentin (Vim) and the transcription factors (Snail, Zeb1 Twist and Slug) were further detected at mRNA and protein levels by qRT-PCR and Western blotting, respectively. The results showed that ERRα promoted the growth of lung cancer A549 cells in vitro. XCT-790 significantly inhibited the migration and invasion of A549 cells. Over-expression of ERRα promoted the epithelial-to-mesenchymal transition (EMT) of A549 cells, down-regulated the epithelial makers E-Cad and ZO-1, and up-regulated the mesenchymal makers FN and Vim. Silencing of Slug, but not other transcription factors, significantly abolished the ERRα-induced EMT of A549 cells. It was suggested that ERRα promoted the migration and invasion of A549 cells by inducing EMT, and Slug was involved in the process. Targeting ERRα might be an efficient approach for lung cancer treatment.
         datePublished:2014-12-06T00:00:00Z
         dateModified:2014-12-06T00:00:00Z
         pageStart:875
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            name:Journal of Huazhong University of Science and Technology [Medical Sciences]
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ScholarlyArticle:
      headline:Effects of estrogen-related receptor alpha (ERRα) on proliferation and metastasis of human lung cancer A549 cells
      description:Estrogen-related receptor alpha (ERRα) plays an important role in the development of hormone-dependent cancers, but its roles in lung cancer remain elusive. The present study was aimed to investigate the effects of ERRα on the proliferation and metastasis of lung cancer A549 cells. The mRNA and protein levels of ERRα were detected in lung cancer A549 and MCF-7 cells and bronchial epithelial BEAS-2B cells by qRT-PCR and Western blotting, respectively. ERRα plasmid transfection and XCT-790 (an inverse agonist of ERRα) were used to up-regulate or down-regulate ERRα expression in A549 cells, respectively. The viability of A549 cells was measured by cell counting kit-8 (CCK-8) and the motility of A549 cells by wound healing assay and Transwell migration/invasion assay. The epithelial markers E-cadherin (E-Cad) and zona occludin-1 (ZO-1), the mesenchymal markers fibronectin (FN) and vimentin (Vim) and the transcription factors (Snail, Zeb1 Twist and Slug) were further detected at mRNA and protein levels by qRT-PCR and Western blotting, respectively. The results showed that ERRα promoted the growth of lung cancer A549 cells in vitro. XCT-790 significantly inhibited the migration and invasion of A549 cells. Over-expression of ERRα promoted the epithelial-to-mesenchymal transition (EMT) of A549 cells, down-regulated the epithelial makers E-Cad and ZO-1, and up-regulated the mesenchymal makers FN and Vim. Silencing of Slug, but not other transcription factors, significantly abolished the ERRα-induced EMT of A549 cells. It was suggested that ERRα promoted the migration and invasion of A549 cells by inducing EMT, and Slug was involved in the process. Targeting ERRα might be an efficient approach for lung cancer treatment.
      datePublished:2014-12-06T00:00:00Z
      dateModified:2014-12-06T00:00:00Z
      pageStart:875
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         XCT-790
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         name:Journal of Huazhong University of Science and Technology [Medical Sciences]
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            1993-1352
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            Periodical
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         name:Huazhong University of Science and Technology
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                     name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Bao-zhang Guan
            affiliation:
                  name:The First Affiliated Hospital of Jinan University
                  address:
                     name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
                     type:PostalAddress
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                     type:PostalAddress
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               type:PostalAddress
            type:Organization
      name:Bao-zhang Guan
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            name:The First Affiliated Hospital of Jinan University
            address:
               name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
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            name:The First Affiliated Hospital of Jinan University
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      name:Bo Hu
      affiliation:
            name:The First Affiliated Hospital of Jinan University
            address:
               name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
               type:PostalAddress
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      affiliation:
            name:The First Affiliated Hospital of Jinan University
            address:
               name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Fo-lan Li
      affiliation:
            name:The First Affiliated Hospital of Jinan University
            address:
               name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
               type:PostalAddress
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            name:The First Affiliated Hospital of Jinan University
            address:
               name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
               type:PostalAddress
            type:Organization
      name:Yu Chen
      affiliation:
            name:The First Affiliated Hospital of Jinan University
            address:
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      name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
      name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
      name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
      name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
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      name:Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China
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