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siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells

Received: 14 September 2020     Accepted: 29 September 2020     Published: 16 October 2020
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Abstract

MDS1 and EVI1 complex locus protein EVI1 (MECOM) is an oncogenic transcription factor in many types of cancer. However, the clinical significance of MECOM in esophagogastric cancer has not been well elucidated. The aim of this study was to define the association of amplification of MECOM and esophagogastric cancer patients’ overall survival rate and to investigate the functional role of MECOM in MKN45 cell proliferation and apoptosis. In this study, a total of 3236 esophagus and gastric patients were analyzed from 16 genomic studies using cBioPortal, which provides an open-access resource with multiple cancer genomics data sets. When the patient samples were divided into two subgroups (MECOM amplified group and MECOM non-amplified group), the poor survival rate was significantly associated with MECOM amplification (p= 0.04). To investigate the role of EVI1 on esophagogastric cancer cells, siRNA dependent gene silencing of EVI1 in MKN45 cells was conducted. RT-PCR was used to examine the expression of EVI1 in MKN45 cells. The MTT assay was used to examine cell proliferation. The apoptotic cells were quantified by fluorescence cell counter. Knockdown of EVI1 leads to reduced cell proliferation and induced apoptosis in MKN45 cells. These results indicate that MECOM may be a potential target for esophagus and gastric cancer gene-targeted therapy. Collectively, our result suggested that EVI1 is a probable target gene for esophagogastric cancer cell proliferation.

Published in Cell Biology (Volume 8, Issue 2)
DOI 10.11648/j.cb.20200802.12
Page(s) 27-32
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2020. Published by Science Publishing Group

Keywords

MECOM, Esophagogastric Cancer, siRNA, RT-PCR, Cell Proliferation, Apoptosis

References
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Cite This Article
  • APA Style

    Yuri Na, Hyejun Hwang, Jaehyuk Cho, Woo Rin Lee. (2020). siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells. Cell Biology, 8(2), 27-32. https://doi.org/10.11648/j.cb.20200802.12

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    ACS Style

    Yuri Na; Hyejun Hwang; Jaehyuk Cho; Woo Rin Lee. siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells. Cell Biol. 2020, 8(2), 27-32. doi: 10.11648/j.cb.20200802.12

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    AMA Style

    Yuri Na, Hyejun Hwang, Jaehyuk Cho, Woo Rin Lee. siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells. Cell Biol. 2020;8(2):27-32. doi: 10.11648/j.cb.20200802.12

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  • @article{10.11648/j.cb.20200802.12,
      author = {Yuri Na and Hyejun Hwang and Jaehyuk Cho and Woo Rin Lee},
      title = {siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells},
      journal = {Cell Biology},
      volume = {8},
      number = {2},
      pages = {27-32},
      doi = {10.11648/j.cb.20200802.12},
      url = {https://doi.org/10.11648/j.cb.20200802.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20200802.12},
      abstract = {MDS1 and EVI1 complex locus protein EVI1 (MECOM) is an oncogenic transcription factor in many types of cancer. However, the clinical significance of MECOM in esophagogastric cancer has not been well elucidated. The aim of this study was to define the association of amplification of MECOM and esophagogastric cancer patients’ overall survival rate and to investigate the functional role of MECOM in MKN45 cell proliferation and apoptosis. In this study, a total of 3236 esophagus and gastric patients were analyzed from 16 genomic studies using cBioPortal, which provides an open-access resource with multiple cancer genomics data sets. When the patient samples were divided into two subgroups (MECOM amplified group and MECOM non-amplified group), the poor survival rate was significantly associated with MECOM amplification (p= 0.04). To investigate the role of EVI1 on esophagogastric cancer cells, siRNA dependent gene silencing of EVI1 in MKN45 cells was conducted. RT-PCR was used to examine the expression of EVI1 in MKN45 cells. The MTT assay was used to examine cell proliferation. The apoptotic cells were quantified by fluorescence cell counter. Knockdown of EVI1 leads to reduced cell proliferation and induced apoptosis in MKN45 cells. These results indicate that MECOM may be a potential target for esophagus and gastric cancer gene-targeted therapy. Collectively, our result suggested that EVI1 is a probable target gene for esophagogastric cancer cell proliferation.},
     year = {2020}
    }
    

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  • TY  - JOUR
    T1  - siRNA-dependent Gene Silencing of EVI1 Decreased Cell Proliferation in MKN45 Cells
    AU  - Yuri Na
    AU  - Hyejun Hwang
    AU  - Jaehyuk Cho
    AU  - Woo Rin Lee
    Y1  - 2020/10/16
    PY  - 2020
    N1  - https://doi.org/10.11648/j.cb.20200802.12
    DO  - 10.11648/j.cb.20200802.12
    T2  - Cell Biology
    JF  - Cell Biology
    JO  - Cell Biology
    SP  - 27
    EP  - 32
    PB  - Science Publishing Group
    SN  - 2330-0183
    UR  - https://doi.org/10.11648/j.cb.20200802.12
    AB  - MDS1 and EVI1 complex locus protein EVI1 (MECOM) is an oncogenic transcription factor in many types of cancer. However, the clinical significance of MECOM in esophagogastric cancer has not been well elucidated. The aim of this study was to define the association of amplification of MECOM and esophagogastric cancer patients’ overall survival rate and to investigate the functional role of MECOM in MKN45 cell proliferation and apoptosis. In this study, a total of 3236 esophagus and gastric patients were analyzed from 16 genomic studies using cBioPortal, which provides an open-access resource with multiple cancer genomics data sets. When the patient samples were divided into two subgroups (MECOM amplified group and MECOM non-amplified group), the poor survival rate was significantly associated with MECOM amplification (p= 0.04). To investigate the role of EVI1 on esophagogastric cancer cells, siRNA dependent gene silencing of EVI1 in MKN45 cells was conducted. RT-PCR was used to examine the expression of EVI1 in MKN45 cells. The MTT assay was used to examine cell proliferation. The apoptotic cells were quantified by fluorescence cell counter. Knockdown of EVI1 leads to reduced cell proliferation and induced apoptosis in MKN45 cells. These results indicate that MECOM may be a potential target for esophagus and gastric cancer gene-targeted therapy. Collectively, our result suggested that EVI1 is a probable target gene for esophagogastric cancer cell proliferation.
    VL  - 8
    IS  - 2
    ER  - 

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Author Information
  • Albany Academy for Girls, New York, The United States of America

  • North London Collegiate School Jeju, Jeju, Republic of Korea

  • Holy Cross High School, New York, The United States of America

  • Department Biological Science, University of Suwon, Hwaseong, Republic of Korea

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