We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
SMARCAD1 in Breast Cancer Progression.
- Authors
Arafat, Kholoud; Al Kubaisy, Elham; Sulaiman, Shahrazad; Attoub, Samir; Karam, Sherif M.; Al Natour, Zeina; Hassan, Ahmed H.
- 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 IKKp expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.
- Subjects
BREAST cancer; CELL proliferation; TUMOR growth; TRIPLE-negative breast cancer; ANTINEOPLASTIC agents
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2018, Vol 50, Issue 2, p489
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000494163