microRNA-29 negatively regulates EMT regulator N-myc interactor in breast cancer
نویسندگان
چکیده
منابع مشابه
N-Myc and STAT Interactor regulates autophagy and chemosensitivity in breast cancer cells
We have previously reported that expression of NMI (N-myc and STAT interactor) is compromised in invasive breast cancers. We also demonstrated that loss of NMI expression promotes epithelial-mesenchymal-transition and results in enhanced invasive ability of breast cancer cells. Additionally we had demonstrated that restoration of NMI expression reduced breast cancer xenograft growth and downreg...
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Breast cancer is the most common cancer among women, and the second leading cause of deaths due to cancer in the US [1]. About 90% of deaths from cancer are due to metastasis, a complex process in which tumor cells escape the primary local tumor, invade through surrounding tissues to spread and colonize distant organs. Tumor cells frequently undergo epithelial-to-mesenchymal transition (EMT), a...
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N-myc & STAT Interactor, NMI, is a protein that has mostly been studied for its physical interactions with transcription factors that play critical roles in tumor growth, progression and metastasis. NMI is an inducible protein, thus its intracellular levels and location can vary dramatically, influencing a diverse array of cellular functions in a context-dependent manner. The physical interacti...
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Breast cancer resistance protein (BCRP/ABCG2) is a molecular determinant of pharmacokinetic properties of many drugs in humans. To understand post-transcriptional regulation of ABCG2 and the role of microRNAs (miRNAs) in drug disposition, we found that microRNA-328 (miR-328) might readily target the 3'-untranslated region (3'-UTR) of ABCG2 when considering target-site accessibility. We then not...
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ژورنال
عنوان ژورنال: Molecular Cancer
سال: 2014
ISSN: 1476-4598
DOI: 10.1186/1476-4598-13-200