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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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  11. Analytics And Tracking
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We are analyzing https://link.springer.com/article/10.1007/s12032-024-02313-9.

Title:
Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights | Medical Oncology
Description:
Oral squamous cell carcinoma (OSCC) is a cancer type with a high rate of recurrence and a poor prognosis. Tumor chemo-resistance remains an issue for OSCC patients despite the availability of multimodal therapy options, which causes an increase in tumor invasiveness. Vacuolar ATPase (V-ATPase), appears to be one of the most significant molecules implicated in MDR in tumors like OSCC. It is primarily responsible for controlling the acidity in the solid tumors’ microenvironment, which interferes with the absorption of chemotherapeutic medications. However, the exact cellular and molecular mechanisms V-ATPase plays in OSCC chemo-resistance have not been understood. Uncovering these mechanisms can contribute to combating OSCC chemo-resistance and poor prognosis. Hence, in this review, we suggest that one of these underlying mechanisms is autophagy induced by V-ATPase which can potentially contribute to OSCC chemo-resistance. Finally, specialized autophagy and V-ATPase inhibitors may be beneficial as an approach to reduce drug resistance to anticancer therapies in addition to serving as coadjuvants in antitumor treatments. Also, V-ATPase could be a prognostic factor for OSCC patients. However, in the future, more investigations are required to demonstrate these suggestions and hypotheses.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

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 {📈}

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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

pubmed, article, google, scholar, cas, cell, cancer, oral, central, carcinoma, squamous, autophagy, resistance, vatpase, tumor, vacuolar, cells, chemoresistance, chen, biol, role, metastasis, liu, wang, drug, oncol, hatpase, physiol, carbonic, tumors, university, res, oscc, microenvironment, vatpases, zhang, mol, patients, atpase, mechanisms, inhibitors, antitumor, treatment, front, zhou, int, sci, human, expression, anhydrase,

Topics {✒️}

mn-based cgas-sting activation camkk2/ampk/mtor signaling pathway pi3k/akt/mtor signaling pathway month download article/chapter increased v-atpase activity hypoxia-regulated carbonic anhydrase-9 multi-territory perforator flaps mohsen nabi-afjadi kdm4c-mediated chromatin modifications tumor chemo-resistance remains selected v-atpase domains proton-motive force generation rewiring chaperone-mediated autophagy targeting epithelial-mesenchymal transition combating oscc chemo-resistance trail-induced cell death resistant ovarian cancer specific v-atpase inhibitors caspase-independent apoptotic pathway anti-cancer drug discovery multi-cup dissolution approach miro1-mediated mitophagy inhibition suppressing beclin1-mediated autophagy plasma membrane v-atpases v-atpase-mediated acidification extracellular vesicle-mediated chemoresistance transmembrane carbonic anhydrases rankl triggers resistance tufts university-graduate school carbonic anhydrases ix carbonic anhydrase ix full article pdf carbonic anhydrase inhibitors melika sadat haeri anti-tumor effect squamous cell head ph gradient reversal increased exosome release altering mitochondrial fission privacy choices/manage cookies breast cancer cells bone sarcomas cancers oscc chemo-resistance inhibiting chemo-resistance pérez-sayáns carbonic anhydrase xii epithelial-mesenchymal transition chemo-radio resistance v-atpase inhibitors cancer therapy access

Questions {❓}

  • Autophagy modulation: a prudent approach in cancer treatment?
  • What is pH regulation, and why do cancer cells need it?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights
         description:Oral squamous cell carcinoma (OSCC) is a cancer type with a high rate of recurrence and a poor prognosis. Tumor chemo-resistance remains an issue for OSCC patients despite the availability of multimodal therapy options, which causes an increase in tumor invasiveness. Vacuolar ATPase (V-ATPase), appears to be one of the most significant molecules implicated in MDR in tumors like OSCC. It is primarily responsible for controlling the acidity in the solid tumors’ microenvironment, which interferes with the absorption of chemotherapeutic medications. However, the exact cellular and molecular mechanisms V-ATPase plays in OSCC chemo-resistance have not been understood. Uncovering these mechanisms can contribute to combating OSCC chemo-resistance and poor prognosis. Hence, in this review, we suggest that one of these underlying mechanisms is autophagy induced by V-ATPase which can potentially contribute to OSCC chemo-resistance. Finally, specialized autophagy and V-ATPase inhibitors may be beneficial as an approach to reduce drug resistance to anticancer therapies in addition to serving as coadjuvants in antitumor treatments. Also, V-ATPase could be a prognostic factor for OSCC patients. However, in the future, more investigations are required to demonstrate these suggestions and hypotheses.
         datePublished:2024-04-09T00:00:00Z
         dateModified:2024-04-09T00:00:00Z
         pageStart:1
         pageEnd:13
         sameAs:https://doi.org/10.1007/s12032-024-02313-9
         keywords:
            Oral cancer
            OSCC
            V-ATPase
            Chemo-resistance
            Autophagy
            Chemotherapy
            Oncology
            Hematology
            Pathology
            Internal Medicine
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         isPartOf:
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            issn:
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            volumeNumber:41
            type:
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                     address:
                        name:Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran
                        type:PostalAddress
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               name:Marziye Askari
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                     name:Hamedan University of Medical Sciences
                     address:
                        name:Department of Immunology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
                        type:PostalAddress
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               name:Melika Sadat Haeri
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                        type:PostalAddress
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                        name:Biotechnology Department, Biological Sciences Faculty, Alzahra University, Tehran, Iran
                        type:PostalAddress
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               name:Sara Banihashemi
               affiliation:
                     name:Nottingham Trend University
                     address:
                        name:Department of Bioscience, School of Science and Technology, Nottingham Trend University, Nottingham, UK
                        type:PostalAddress
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               name:Mohsen Nabi-Afjadi
               url:http://orcid.org/0000-0001-8243-1530
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                     name:Tarbiat Modares University
                     address:
                        name:Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
                        type:PostalAddress
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               name:Yalda Malekzadegan
               url:http://orcid.org/0000-0002-4461-9900
               affiliation:
                     name:Saveh University of Medical Sciences
                     address:
                        name:Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran
                        type:PostalAddress
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ScholarlyArticle:
      headline:Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights
      description:Oral squamous cell carcinoma (OSCC) is a cancer type with a high rate of recurrence and a poor prognosis. Tumor chemo-resistance remains an issue for OSCC patients despite the availability of multimodal therapy options, which causes an increase in tumor invasiveness. Vacuolar ATPase (V-ATPase), appears to be one of the most significant molecules implicated in MDR in tumors like OSCC. It is primarily responsible for controlling the acidity in the solid tumors’ microenvironment, which interferes with the absorption of chemotherapeutic medications. However, the exact cellular and molecular mechanisms V-ATPase plays in OSCC chemo-resistance have not been understood. Uncovering these mechanisms can contribute to combating OSCC chemo-resistance and poor prognosis. Hence, in this review, we suggest that one of these underlying mechanisms is autophagy induced by V-ATPase which can potentially contribute to OSCC chemo-resistance. Finally, specialized autophagy and V-ATPase inhibitors may be beneficial as an approach to reduce drug resistance to anticancer therapies in addition to serving as coadjuvants in antitumor treatments. Also, V-ATPase could be a prognostic factor for OSCC patients. However, in the future, more investigations are required to demonstrate these suggestions and hypotheses.
      datePublished:2024-04-09T00:00:00Z
      dateModified:2024-04-09T00:00:00Z
      pageStart:1
      pageEnd:13
      sameAs:https://doi.org/10.1007/s12032-024-02313-9
      keywords:
         Oral cancer
         OSCC
         V-ATPase
         Chemo-resistance
         Autophagy
         Chemotherapy
         Oncology
         Hematology
         Pathology
         Internal Medicine
      image:
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs12032-024-02313-9/MediaObjects/12032_2024_2313_Fig3_HTML.png
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            1559-131X
         volumeNumber:41
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         name:Springer US
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            name:Ahmadreza Lagzian
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                  name:University of Tehran
                  address:
                     name:Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Marziye Askari
            affiliation:
                  name:Hamedan University of Medical Sciences
                  address:
                     name:Department of Immunology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Melika Sadat Haeri
            affiliation:
                  name:Islamic Azad University
                  address:
                     name:Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nastaran Sheikhi
            affiliation:
                  name:Alzahra University
                  address:
                     name:Biotechnology Department, Biological Sciences Faculty, Alzahra University, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Sara Banihashemi
            affiliation:
                  name:Nottingham Trend University
                  address:
                     name:Department of Bioscience, School of Science and Technology, Nottingham Trend University, Nottingham, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Mohsen Nabi-Afjadi
            url:http://orcid.org/0000-0001-8243-1530
            affiliation:
                  name:Tarbiat Modares University
                  address:
                     name:Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Yalda Malekzadegan
            url:http://orcid.org/0000-0002-4461-9900
            affiliation:
                  name:Saveh University of Medical Sciences
                  address:
                     name:Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran
                     type:PostalAddress
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      name:Medical Oncology
      issn:
         1559-131X
      volumeNumber:41
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      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Tehran
      address:
         name:Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran
         type:PostalAddress
      name:Hamedan University of Medical Sciences
      address:
         name:Department of Immunology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
         type:PostalAddress
      name:Islamic Azad University
      address:
         name:Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
         type:PostalAddress
      name:Alzahra University
      address:
         name:Biotechnology Department, Biological Sciences Faculty, Alzahra University, Tehran, Iran
         type:PostalAddress
      name:Nottingham Trend University
      address:
         name:Department of Bioscience, School of Science and Technology, Nottingham Trend University, Nottingham, UK
         type:PostalAddress
      name:Tarbiat Modares University
      address:
         name:Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
         type:PostalAddress
      name:Saveh University of Medical Sciences
      address:
         name:Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran
         type:PostalAddress
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      affiliation:
            name:University of Tehran
            address:
               name:Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Marziye Askari
      affiliation:
            name:Hamedan University of Medical Sciences
            address:
               name:Department of Immunology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
               type:PostalAddress
            type:Organization
      name:Melika Sadat Haeri
      affiliation:
            name:Islamic Azad University
            address:
               name:Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Nastaran Sheikhi
      affiliation:
            name:Alzahra University
            address:
               name:Biotechnology Department, Biological Sciences Faculty, Alzahra University, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Sara Banihashemi
      affiliation:
            name:Nottingham Trend University
            address:
               name:Department of Bioscience, School of Science and Technology, Nottingham Trend University, Nottingham, UK
               type:PostalAddress
            type:Organization
      name:Mohsen Nabi-Afjadi
      url:http://orcid.org/0000-0001-8243-1530
      affiliation:
            name:Tarbiat Modares University
            address:
               name:Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yalda Malekzadegan
      url:http://orcid.org/0000-0002-4461-9900
      affiliation:
            name:Saveh University of Medical Sciences
            address:
               name:Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran
      name:Department of Immunology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
      name:Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
      name:Biotechnology Department, Biological Sciences Faculty, Alzahra University, Tehran, Iran
      name:Department of Bioscience, School of Science and Technology, Nottingham Trend University, Nottingham, UK
      name:Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
      name:Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran
WebPageElement:
      isAccessibleForFree:
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External Links {🔗}(381)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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