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The role of Nanog expression in tamoxifen-resistant breast cancer cells

Version 4 2024-03-12, 13:32
Version 3 2023-10-29, 10:00
journal contribution
posted on 2024-03-12, 13:32 authored by Khalid Arif, Issam HussainIssam Hussain, Carol ReaCarol Rea, Mohamed El-Sheemy

There is an accumulation of evidence that shows a significant role of cancer stem cells in tumor initiation, proliferation, relapse, and metastasis. Nanog is the most important core transcription marker of stem cells, known by its role in maintaining pluripotency, proliferation, and differentiation. Therefore, this study aimed to examine the role of Nanog in breast cancer cell tamoxifen resistance and its implications in breast cancer treatment. In this study, the expression of the three core transcription markers Nanog, Oct3/4, and Sox2 were quantitatively evaluated using flow cytometry. Then, small interfering RNA (siRNA) against human Nanog was transfected into tamoxifen-resistant breast cancer cells via Lipofectamine 2000. Nanog gene expression in the cells was detected using reverse transcription polymerase chain reaction (RT-PCR). The change in cell proliferation was evaluated using the tetrazolium bromide method. An enzyme-linked immunosorbent assay was used to detect apoptosis of the transfected cells alone and in combination with 4-hydroxytamoxifen. The results showed a high level expression of Nanog, Oct3/4, and Sox2 in MDA-MB-231 and MCF7/tamoxifen resistant cells compared with MCF7/wild-type. siRNA-mediated Nanog gene silencing can efficiently inhibit cell proliferation and induce apoptosis of tamoxifen-resistant breast cancer cells. This study provides a basis for further study of the role of Nanog in developing resistance to tamoxifen, its implication in breast cancer management, and as a new strategy to enhance response to endocrine therapy.

History

School affiliated with

  • Department of Life Sciences (Research Outputs)

Publication Title

OncoTargets and Therapy

Volume

8

Pages/Article Number

1327-1334

Publisher

Dove Medical Press

ISSN

1178-6930

eISSN

1178-6930

Date Submitted

2015-07-10

Date Accepted

2014-10-01

Date of First Publication

2015-06-03

Date of Final Publication

2015-06-03

Date Document First Uploaded

2015-07-10

ePrints ID

17779

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