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المؤلفAlateyah, Nouralhuda
المؤلفGupta, Ishita
المؤلفRusyniak, Radoslaw Stefan
المؤلفOuhtit, Allal
تاريخ الإتاحة2022-03-13T06:51:54Z
تاريخ النشر2022-02-01
اسم المنشورMolecules
المعرّفhttp://dx.doi.org/10.3390/molecules27030811
الاقتباسAlateyah, N.; Gupta, I.; Rusyniak, R.S.; Ouhtit, A. SOD2, a Potential Transcriptional Target Underpinning CD44-Promoted Breast Cancer Progression. Molecules 2022, 27, 811. https://doi.org/ 10.3390/molecules27030811
معرّف المصادر الموحدhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85123508438&origin=inward
معرّف المصادر الموحدhttp://hdl.handle.net/10576/27993
الملخصCD44, a cell-adhesion molecule has a dual role in tumor growth and progression; it acts as a tumor suppressor as well as a tumor promoter. In our previous work, we developed a tetracycline-off regulated expression of CD44’s gene in the breast cancer (BC) cell line MCF-7 (B5 clone). Using cDNA oligo gene expression microarray, we identified SOD2 (superoxide dismutase 2) as a potential CD44-downstream transcriptional target involved in BC metastasis. SOD2 gene belongs to the family of iron/manganese superoxide dismutase family and encodes a mitochondrial protein. SOD2 plays a role in cell proliferation and cell invasion via activation of different signaling pathways regulating angiogenic abilities of breast tumor cells. This review will focus on the findings supporting the underlying mechanisms associated with the oncogenic potential of SOD2 in the onset and progression of cancer, especially in BC and the potential clinical relevance of its various inhibitors.
راعي المشروعThis research was funded by Qatar University Internal grant number: QUST-1-CAS2019-22, QUST-2-CAS-2021-137 and QUST-2-CAS-2021-138 and, the Qatar Foundation grant number: UREP24-117-1-027. Open Access funding was provided by the Qatar National Library.
اللغةen
الناشرMDPI
الموضوعBreast cancer
CD44
Hyaluronan
Invasion
SOD2
العنوانSOD2, a Potential Transcriptional Target Underpinning CD44-Promoted Breast Cancer Progression
النوعArticle Review
رقم العدد3
رقم المجلد27
ESSN1420-3049
dc.accessType Open Access


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