In vitro transfection of anti-tumor miR-101 induces BIM, a pro-apoptotic protein, expression in acute myeloid leukemia (AML)

Authors

  • Narges Nikoonahad Lotfabadi Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran; Biology Department, Faculty of Sciences, Science and Arts University, Yazd, Iran
  • Homa Mohseni Kouchesfahani Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
  • Mohammad Hasan Sheikhha Reproductive & Genetic Unit, Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran; Biotechnology Research Center, International Campus, Shahid Sadoughi University of Medical Science, Yazd, Iran
  • Seyed Mehdi Kalantar Reproductive & Genetic Unit, Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran

DOI:

https://doi.org/10.17179/excli2017-721

Keywords:

AML, miR-101, BIM, apoptosis

Abstract

Acute myeloid leukemia (AML) frequently relapses after initial treatment, though it is possible that drug resistance occurs. Hence, it seems necessary to develop novel therapies such as gene therapy specifically via miRNA transfection. MicroRNA-101 has been considered as a tumor suppressor in different types of cancer. It is demonstrated that exogenous miR-101 transfection is associated with decreased viability in AML in this paper. Besides, the increase of pro-apoptotic protein BIM expression in both mRNA and protein level has been illustrated. The recent findings provide an insight into the novel function of miR-101 in AML by activating BIM as an important mediator in intrinsic apoptosis pathways. Generally, miR-101 has been considered as a therapeutic target in our data and might have a valuable role in AML.

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Published

2017-11-27

How to Cite

Nikoonahad Lotfabadi, N., Mohseni Kouchesfahani, H., Sheikhha, M. H., & Kalantar, S. M. (2017). In vitro transfection of anti-tumor miR-101 induces BIM, a pro-apoptotic protein, expression in acute myeloid leukemia (AML). EXCLI Journal, 16, 1257–1267. https://doi.org/10.17179/excli2017-721

Issue

Vol. 16 (2017)

Section

Original articles

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