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We are analyzing https://link.springer.com/article/10.1186/s12943-019-1128-6.

Title:
m6A demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling | Molecular Cancer
Description:
Background Pancreatic cancer is one of the most lethal types of cancer with extremely poor diagnosis and prognosis, and chemo-resistance remains a major challenge. The dynamic and reversible N6-methyladenosine (m6A) RNA modification has emerged as a new layer of epigenetic gene regulation. Methods qRT-PCR and IHC were applied to examine ALKBH5 levels in normal and pancreatic cancer tissues. Cancer cell proliferation and chemo-resistance were evaluated by clonogenic formation, chemosensitivity detection, and Western blotting assays. m6A-seq was performed to identify target genes. We evaluated the inhibitory effect of ALKBH5 in both in vivo and in vitro models. Results Here, we show that m6A demethylase ALKBH5 is downregulated in gemcitabine-treated patient-derived xenograft (PDX) model and its overexpression sensitized pancreatic ductal adenocarcinoma (PDAC) cells to chemotherapy. Decreased ALKBH5 levels predicts poor clinical outcome in PDAC and multiple other cancers. Furthermore, silencing ALKBH5 remarkably increases PDAC cell proliferation, migration, and invasion both in vitro and in vivo, whereas its overexpression causes the opposite effects. Global m6A profile revealed altered expression of certain ALKBH5 target genes, including Wnt inhibitory factor 1 (WIF-1), which is correlated with WIF-1 transactivation and mediation of the Wnt pathway. Conclusions Our work uncovers the tumor suppressive and chemo-sensitizing function for ALKBH5, which provides insight into critical roles of m6A methylation in PDAC.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Science
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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 7,626,182 visitors per month in the current month.

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How Does Link.springer.com Make Money? {šŸ’ø}

The income method remains a mystery to us.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {šŸ”}

alkbh, cells, cancer, wif, expression, pdac, fig, article, wnt, cell, pancreatic, google, scholar, signaling, additional, file, gemcitabine, figure, overexpression, aspc, tumor, modification, rna, bxpc, mrna, levels, mmp, mia, mice, control, cas, proliferation, protein, xenograft, paca, formation, data, qrtpcr, human, colony, wang, migration, treatment, methylation, genes, cancers, panc, quantification, analysis, invasion,

Topics {āœ’ļø}

augmented wnt/pi3k-akt signaling gemcitabine-treated patient-derived xenograft poly-a-purified rna heat-induced antigen recovery treated-patient-derived xenograft article download pdf twisted developmental biology article  google scholar wnt/beta-catenin pathway wnt/beta-catenin signaling wnt/β-catenin pathway avidin-biotin peroxidase complex wnt/β-catenin signaling [27 wnt/β-catenin signaling considered statistically significant β-catenin protein levels kaplan-meier analysis indicating network-based methods alkbh5-mediated m6a modification m6a-seq m6a-ip gemcitabine-treated pdx model biological processes including β-catenin mrna transcripts anti-α-catenin antibody pancreatic cancer stem paraffin-embedded tissues cut genes differentially expressed mia paca-2-alkbh5 cells mediating wnt signaling pancreatic ductal adenocarcinoma pancreatic cancer cells targeting beta-catenin including cell proliferation cancer cell proliferation m6a demethylase alkbh5 human colorectal carcinoma human neuroendocrine tumors pancreatic cancer tissues increased cell proliferation cancer stem cell cancer stem cell diminished promoter activations related subjects mediating methylation reversal privacy choices/manage cookies β-catenin promoter activity n6-methyladenosine mettl3 cell proliferation program tumor growth rate nat rev cancer

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:m6A demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling
         description:Pancreatic cancer is one of the most lethal types of cancer with extremely poor diagnosis and prognosis, and chemo-resistance remains a major challenge. The dynamic and reversible N6-methyladenosine (m6A) RNA modification has emerged as a new layer of epigenetic gene regulation. qRT-PCR and IHC were applied to examine ALKBH5 levels in normal and pancreatic cancer tissues. Cancer cell proliferation and chemo-resistance were evaluated by clonogenic formation, chemosensitivity detection, and Western blotting assays. m6A-seq was performed to identify target genes. We evaluated the inhibitory effect of ALKBH5 in both in vivo and in vitro models. Here, we show that m6A demethylase ALKBH5 is downregulated in gemcitabine-treated patient-derived xenograft (PDX) model and its overexpression sensitized pancreatic ductal adenocarcinoma (PDAC) cells to chemotherapy. Decreased ALKBH5 levels predicts poor clinical outcome in PDAC and multiple other cancers. Furthermore, silencing ALKBH5 remarkably increases PDAC cell proliferation, migration, and invasion both in vitro and in vivo, whereas its overexpression causes the opposite effects. Global m6A profile revealed altered expression of certain ALKBH5 target genes, including Wnt inhibitory factor 1 (WIF-1), which is correlated with WIF-1 transactivation and mediation of the Wnt pathway. Our work uncovers the tumor suppressive and chemo-sensitizing function for ALKBH5, which provides insight into critical roles of m6A methylation in PDAC.
         datePublished:2020-01-06T00:00:00Z
         dateModified:2020-01-06T00:00:00Z
         pageStart:1
         pageEnd:15
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s12943-019-1128-6
         keywords:
            Pancreatic cancer
            m6A methylation
            Chemo-resistance
            ALKBH5
            WIF-1
            Wnt
            Cancer Research
            Oncology
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                        type:PostalAddress
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               name:Min Kang
               affiliation:
                     name:the First Affiliated Hospital of Guangxi Medical University
                     address:
                        name:Department of Radiation Oncology, the First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                        type:PostalAddress
                     type:Organization
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               name:Yunshan Wang
               affiliation:
                     name:The Second Hospital of Shandong University
                     address:
                        name:Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, China
                        type:PostalAddress
                     type:Organization
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               affiliation:
                     name:The First Affiliated Hospital of Guangxi Medical University
                     address:
                        name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                        type:PostalAddress
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                     name:The First Affiliated Hospital of Guangxi Medical University
                     address:
                        name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                        type:PostalAddress
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               name:Songqing He
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                     name:The First Affiliated Hospital of Guangxi Medical University
                     address:
                        name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                        type:PostalAddress
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               name:Fumio Shimamoto
               affiliation:
                     name:Hiroshima Shudo University
                     address:
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      headline:m6A demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling
      description:Pancreatic cancer is one of the most lethal types of cancer with extremely poor diagnosis and prognosis, and chemo-resistance remains a major challenge. The dynamic and reversible N6-methyladenosine (m6A) RNA modification has emerged as a new layer of epigenetic gene regulation. qRT-PCR and IHC were applied to examine ALKBH5 levels in normal and pancreatic cancer tissues. Cancer cell proliferation and chemo-resistance were evaluated by clonogenic formation, chemosensitivity detection, and Western blotting assays. m6A-seq was performed to identify target genes. We evaluated the inhibitory effect of ALKBH5 in both in vivo and in vitro models. Here, we show that m6A demethylase ALKBH5 is downregulated in gemcitabine-treated patient-derived xenograft (PDX) model and its overexpression sensitized pancreatic ductal adenocarcinoma (PDAC) cells to chemotherapy. Decreased ALKBH5 levels predicts poor clinical outcome in PDAC and multiple other cancers. Furthermore, silencing ALKBH5 remarkably increases PDAC cell proliferation, migration, and invasion both in vitro and in vivo, whereas its overexpression causes the opposite effects. Global m6A profile revealed altered expression of certain ALKBH5 target genes, including Wnt inhibitory factor 1 (WIF-1), which is correlated with WIF-1 transactivation and mediation of the Wnt pathway. Our work uncovers the tumor suppressive and chemo-sensitizing function for ALKBH5, which provides insight into critical roles of m6A methylation in PDAC.
      datePublished:2020-01-06T00:00:00Z
      dateModified:2020-01-06T00:00:00Z
      pageStart:1
      pageEnd:15
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-019-1128-6
      keywords:
         Pancreatic cancer
         m6A methylation
         Chemo-resistance
         ALKBH5
         WIF-1
         Wnt
         Cancer Research
         Oncology
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      author:
            name:Bo Tang
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                     type:PostalAddress
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            type:Person
            name:Yihua Yang
            affiliation:
                  name:The First Affiliated Hospital of Guangxi Medical University
                  address:
                     name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Min Kang
            affiliation:
                  name:the First Affiliated Hospital of Guangxi Medical University
                  address:
                     name:Department of Radiation Oncology, the First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yunshan Wang
            affiliation:
                  name:The Second Hospital of Shandong University
                  address:
                     name:Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yan Wang
            affiliation:
                  name:The First Affiliated Hospital of Guangxi Medical University
                  address:
                     name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Yin Bi
            affiliation:
                  name:The First Affiliated Hospital of Guangxi Medical University
                  address:
                     name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Songqing He
            affiliation:
                  name:The First Affiliated Hospital of Guangxi Medical University
                  address:
                     name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Fumio Shimamoto
            affiliation:
                  name:Hiroshima Shudo University
                  address:
                     name:Department of Health Sciences, Hiroshima Shudo University, Hiroshima, Japan
                     type:PostalAddress
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         name:Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, China
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      name:The First Affiliated Hospital of Guangxi Medical University
      address:
         name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
         type:PostalAddress
      name:The First Affiliated Hospital of Guangxi Medical University
      address:
         name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
         type:PostalAddress
      name:The First Affiliated Hospital of Guangxi Medical University
      address:
         name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
         type:PostalAddress
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      address:
         name:Department of Health Sciences, Hiroshima Shudo University, Hiroshima, Japan
         type:PostalAddress
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      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Bo Tang
      affiliation:
            name:The First Affiliated Hospital of Guangxi Medical University
            address:
               name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yihua Yang
      affiliation:
            name:The First Affiliated Hospital of Guangxi Medical University
            address:
               name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Min Kang
      affiliation:
            name:the First Affiliated Hospital of Guangxi Medical University
            address:
               name:Department of Radiation Oncology, the First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Yunshan Wang
      affiliation:
            name:The Second Hospital of Shandong University
            address:
               name:Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, China
               type:PostalAddress
            type:Organization
      name:Yan Wang
      affiliation:
            name:The First Affiliated Hospital of Guangxi Medical University
            address:
               name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Yin Bi
      affiliation:
            name:The First Affiliated Hospital of Guangxi Medical University
            address:
               name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Songqing He
      affiliation:
            name:The First Affiliated Hospital of Guangxi Medical University
            address:
               name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Fumio Shimamoto
      affiliation:
            name:Hiroshima Shudo University
            address:
               name:Department of Health Sciences, Hiroshima Shudo University, Hiroshima, Japan
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Department of Radiation Oncology, the First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, China
      name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Center of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, People’s Republic of China
      name:Department of Health Sciences, Hiroshima Shudo University, Hiroshima, Japan

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