مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

video

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

sound

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Persian Version

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

View:

319
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Download:

697
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Cites:

Information Journal Paper

Title

Hsa-miR-587 Regulates TGFβ /SMAD Signaling and Promotes Cell Cycle Progression

Pages

  158-164

Abstract

 Objective: Transforming growth factor beta/single mothers against decapentaplegic (TGFβ /SMAD) signaling pathway plays important roles in various biological processes. It acts as a tumor suppressor during the early stages of Cancer progression. Discovering the regulators of this pathway provides important options for therapeutic strategies. Here, we searched for candidate microRNAs (miRNAs) that potentially target the critical components of the TGFβ signaling pathway. Materials and Methods: In the current experimental study, we first predicted miRNAs that target TGFβ components using a bioinformatics software. After that, quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-587, TGFBR2, SMAD4, p21, CCND1 and c-MYC genes in transfected HEK293T and HCT116 cells. Dual Luciferase assay was performed to analyze the interactions between miRNAs and the target genes. Propidium iodide flow cytometry was used to determine Cell Cycle progression in HEK293T and HCT116 cells under hsa-miR-587 (miR-587) overexpression circumstances. Results: Multiple miRNA responsive elements (MREs) were predicted for miR-587 within the 3’ UTRs of the TGFBR2 and SMAD4 genes. Overexpression of miR-587 in HEK293T and HCT116 cells resulted in downregulation of TGFBR2 and SMAD4 genes. In addition, a downstream target gene of TGFβ /SMAD signaling, P21, was significantly downregulated in the HCT116 cells overexpressing miR-587. Dual luciferase assay analysis provided evidence that there is a direct interaction between miR-587 and the 3’ UTR sequences of TGFBR2 and SMAD4 genes. Moreover, miR-587 overexpression in HEK293T and HCT116 cells resulted in reducing the SubG1 cell populations in both cell lines, as detected by flow cytometry. Conclusion: Altogether, our data revealed an important role for miR-587 in regulating TGFβ /SMAD signaling and promoting Cell Cycle progression. These characteristics suggest that miR-587 is an important candidate for Cancer therapy research.

Cites

  • No record.
  • References

    Cite

    APA: Copy

    Jahangirimoez, Mahnaz, Medlej, Abdallah, TAVALAEI, MAHMOUD, & Soltani, Bahram Mohammad. (2020). Hsa-miR-587 Regulates TGFβ /SMAD Signaling and Promotes Cell Cycle Progression. CELL JOURNAL (YAKHTEH), 22(2), 158-164. SID. https://sid.ir/paper/727368/en

    Vancouver: Copy

    Jahangirimoez Mahnaz, Medlej Abdallah, TAVALAEI MAHMOUD, Soltani Bahram Mohammad. Hsa-miR-587 Regulates TGFβ /SMAD Signaling and Promotes Cell Cycle Progression. CELL JOURNAL (YAKHTEH)[Internet]. 2020;22(2):158-164. Available from: https://sid.ir/paper/727368/en

    IEEE: Copy

    Mahnaz Jahangirimoez, Abdallah Medlej, MAHMOUD TAVALAEI, and Bahram Mohammad Soltani, “Hsa-miR-587 Regulates TGFβ /SMAD Signaling and Promotes Cell Cycle Progression,” CELL JOURNAL (YAKHTEH), vol. 22, no. 2, pp. 158–164, 2020, [Online]. Available: https://sid.ir/paper/727368/en

    Related Journal Papers

  • No record.
  • Related Seminar Papers

  • No record.
  • Related Plans

  • No record.
  • Recommended Workshops






    Move to top
    telegram sharing button
    whatsapp sharing button
    linkedin sharing button
    twitter sharing button
    email sharing button
    email sharing button
    email sharing button
    sharethis sharing button