Silencing of nucleostemin by siRNA induces apoptosis in MCF-7 and MDA-MB-468 cell lines

Document Type : Research article

Authors

1 Genetics of Non-Communicable Disease Research Center, Zahedan University of Medical Sciences, Zahedan, Iran.

2 Department of Medical Genetic, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

3 Cellular and Molecular Research Center, and 3Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran.

4 Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran.

5 Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, Iran.

Abstract

One of the most important modulators involved in controlling apoptosis induction and viability of cancerous cells is nucleostemin. Some studies revealed that NS is also needed to maintain the proliferation of embryonic neural stem cells and early embryogenesis. This study was designed to better elucidate the association between NS depletion status and apoptosis induction of both MCF-7 and MDA-MB-468 cell lines. We examined the effects of nucleostemin-targeting siRNA on the expression of NS in MCF-7 and MDA-MB-468 human breast cancer cell lines by the Real Time polymerase chain reaction method. In addition, we investigated the correlation between knockdown of NS and viability rates and apoptosis induction in MCF-7 and MDA-MB-468 cell lines using the MTT assay and flow-cytometry technique, respectively. The NS-targeting siRNA inhibited the viability of cells in a dose- and time-dependent manner and induced apoptosis after 48 h in the cells. Thus, consistent with previous articles, this protein can be one of the regulators related to the inhibition of apoptosis and the increased viability of tumor-initiating cells in human breast cancer cell lines as well as other cancers.

Graphical Abstract

Silencing of nucleostemin by siRNA induces apoptosis in MCF-7 and MDA-MB-468 cell lines

Keywords

Main Subjects



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