• Register
  • Login

European Journal of Molecular & Clinical Medicine

  • Home
  • Browse
    • Current Issue
    • By Issue
    • By Subject
    • Keyword Index
    • Author Index
    • Indexing Databases XML
  • Journal Info
    • About Journal
    • Aims and Scope
    • Editorial Board
    • Publication Ethics
    • Indexing and Abstracting
    • Peer Review Process
    • News
  • Guide for Authors
  • Submit Manuscript
  • Contact Us
Advanced Search

Notice

As part of Open Journals’ initiatives, we create website for scholarly open access journals. If you are responsible for this journal and would like to know more about how to use the editorial system, please visit our website at https://ejournalplus.com or
send us an email to info@ejournalplus.com

We will contact you soon

  1. Home
  2. Volume 9, Issue 8
  3. Authors

Online ISSN: 2515-8260

Volume9, Issue8

IDENTIFICATION OF ENDOGENOUS OVEREXPRESSION OF CATALASE, AS A INHIBITOR OF EMT SIGNALLING THE PROGRESSION OF BREAST CANCER.

    Kaviya. S Lavanya Prathap Selvaraj Jayaraman Preetha. S

European Journal of Molecular & Clinical Medicine, 2022, Volume 9, Issue 8, Pages 569-577

  • Show Article
  • Download
  • Cite
  • Statistics
  • Share

Abstract

 
BACKGROUND: Tumor is an abnormal cell growth that spreads to other organs. Breast tumor develops in the tissues of the breastRegular exercise can help to lower the chance of developing breast tumor. For the year 2020, the expected incidence of tumor patients in India was 679,421 (94.1 per 100,000) for males and 712,758 (103.6 per 100,000) for females.. AIM: To analyse the endogenous over the expression of catalase as an inhibitor of EMT signaling in breast tumor through molecular docking.
 
MATERIALS AND METHODS:
            The molecular docking analysis is a bio informatic study conducted in a private dental college. The endogenous substance catalase which is secreted after post exercise is used as our target protein. The interaction of catalase with the proteins relevant to breast tumor namely Vimentin, Beta-catenin, Ecadherin are included for docking analysis. The protein structure is retrieved using protein data bank, Protein protein docking done using patch Dock server followed by visualisation of protein-protein interaction using pymol.
 
RESULT:
             The surface representation of catalase with Vimentin, Beta-catenin and Ecadherin showed good shape complementarity.The results showed that Catalase forms strong interaction with Vimetine, Beta catenin, Ecatherine proteins in terms of hydrogen bond interaction, hydrophobic and non bonded interaction. Through this interaction these proteins might control the overexpression of catalase activity in breast tumor.
 
  CONCLUSION:
           From the obtained result it can be concluded that catalase may have a protective role against breast tumor through its interaction with Vimentin, E-Cadherin, Beta-Catenin. The present study has suggested a possible mechanism of catalase in the inhibitor of EMT signaling in breast tumor.
Keywords:
    Breast tumor exercise Catalase Vimentine Beta-catenin Ecadherin innovative method
  • PDF (486 K)
  • XML
(2022). IDENTIFICATION OF ENDOGENOUS OVEREXPRESSION OF CATALASE, AS A INHIBITOR OF EMT SIGNALLING THE PROGRESSION OF BREAST CANCER.. European Journal of Molecular & Clinical Medicine, 9(8), 569-577.
Kaviya. S; Lavanya Prathap; Selvaraj Jayaraman; Preetha. S. "IDENTIFICATION OF ENDOGENOUS OVEREXPRESSION OF CATALASE, AS A INHIBITOR OF EMT SIGNALLING THE PROGRESSION OF BREAST CANCER.". European Journal of Molecular & Clinical Medicine, 9, 8, 2022, 569-577.
(2022). 'IDENTIFICATION OF ENDOGENOUS OVEREXPRESSION OF CATALASE, AS A INHIBITOR OF EMT SIGNALLING THE PROGRESSION OF BREAST CANCER.', European Journal of Molecular & Clinical Medicine, 9(8), pp. 569-577.
IDENTIFICATION OF ENDOGENOUS OVEREXPRESSION OF CATALASE, AS A INHIBITOR OF EMT SIGNALLING THE PROGRESSION OF BREAST CANCER.. European Journal of Molecular & Clinical Medicine, 2022; 9(8): 569-577.
  • RIS
  • EndNote
  • BibTeX
  • APA
  • MLA
  • Harvard
  • Vancouver
  • Article View: 21
  • PDF Download: 45
  • LinkedIn
  • Twitter
  • Facebook
  • Google
  • Telegram
Journal Information

Publisher:

Email:  editor.ejmcm21@gmail.com

  • Home
  • Glossary
  • News
  • Aims and Scope
  • Privacy Policy
  • Sitemap

 

For Special Issue Proposal : editor.ejmcm21@gmail.com

This journal is licensed under a Creative Commons Attribution 4.0 International (CC-BY 4.0)

Powered by eJournalPlus