What is it about?
The cytoplasmic domain of MUC1-C induces internal survival signals that are essential for the regulation of cell function. However, evidence has shown that there exists a strong correlation in aberrant MUC1 expression and the amplification of the cancer cell development via signaling pathways.
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Why is it important?
In vitro studies have demonstrated that targeting MUC1-C terminal with antagonists is highly synergistic with tamoxifen. These results facilitate a better comprehension in the use of selective MUC1-C inhibitors being in synergy with other therapeutic agents aimed at restoring tamoxifen sensitivity. Moreover, this allows for improved experimental designs for prospective clinical investigations.
Perspectives
Abnormal expression of MUC1 in cancer cells may serve as a target that can assist in inducing the immune system to attack and remove such cells. We hope that our data would motivate researchers in this field to consider 'MUC1-C' in estrogen receptor activities in regards to the development of tamoxifen resistance. Our findings suggest that this might be an incomplete viewpoint that needs to be supported with characterized molecular mechanisms involved in tamoxifen-sensitive breast cancer cells.
Parnaz Merikhian
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This page is a summary of: MUC1 induces tamoxifen resistance in estrogen receptor-positive breast cancer, Expert Review of Anticancer Therapy, June 2017, Taylor & Francis,
DOI: 10.1080/14737140.2017.1340837.
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