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Publication:
SMARCAD1 in Breast Cancer Progression

dc.contributor.authorA. Hassan, Ahmed
dc.date.accessioned2021-08-02T09:31:33Z
dc.date.available2021-08-02T09:31:33Z
dc.date.issued2018-10-11
dc.description.abstractBackground/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.en_US
dc.identifier.other204-2018.46
dc.identifier.urihttps://repository.mbru.ac.ae/handle/1/312
dc.language.isoenen_US
dc.subjectBreast cancer (BC)en_US
dc.subjectSMARCAD1en_US
dc.subjectIKKen_US
dc.subjectCell proliferationen_US
dc.subjectTumor growthen_US
dc.titleSMARCAD1 in Breast Cancer Progressionen_US
dc.typeArticleen_US
dspace.entity.typePublication

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