SMARCAD1 in Breast Cancer Progression

Kholoud Arafat, Elham Al Kubaisy, Shahrazad Sulaiman, Sherif M. Karam, Zeina Al Natour, Ahmed H. Hassan, Samir Attoub

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER - /PR - /HER2 - ) and T47D (ER + /PR +/- /HER2 - ) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.

Original languageEnglish
Pages (from-to)501-511
Number of pages11
JournalCellular Physiology and Biochemistry
Volume50
Issue number2
DOIs
Publication statusPublished - Oct 1 2018

Keywords

  • Breast cancer
  • Cell proliferation
  • IKK
  • SMARCAD1
  • Tumor growth

ASJC Scopus subject areas

  • Physiology

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