Protein Acting As Mediator for HER2-driven Breast Cancer Identified


Researchers at the University of Cincinnati College of Medicine have identified an estrogen-binding protein called MED1 as a critical mediator of HER2-driven breast cancer. This finding could lead to potential therapeutic options.

The MED1 protein is often produced at abnormally high levels in breast cancer cells. In HER2 breast cancer, the human epidermal growth factor receptor 2 (HER2), stopping MED1 production leads to a stopping of the cancer's growth. Findings for this study were printed in the journal Cancer Research.

Breast cancer is normally subdivided into groups based on gene expression for estrogen and can be further subdivided by HER2.

The MED1 protein is a known estrogen receptor coactivator and has been shown to play an important role in estrogen receptor-dependent function in both mammary gland development and, now, breast cancer.

"Interestingly, the MED1 gene is located very close to and amplified together with HER2 in the gene, and the MED1 protein levels are highly linked to HER2-positive breast cancer. Additionally, we've found that HER2 can activate MED1, and MED1 functions as a key 'crosstalk' point between the HER2 and estrogen receptor pathway in the treatment resistance of HER2 and estrogen receptor double positive breast cancer. However, the role and underlying molecular functions of MED1 in HER2-driven breast cancer development and spread is still poorly understood," writes Xiaoting Zhang, PhD, associate professor in the Department of Cancer Biology at the UC College of Medicine, member of the Cincinnati Cancer Center and the UC Cancer Institute and lead author on this study.

By mutating MED1 in and near breast cancer regions, the researchers were able to delay tumor growth and spread. The researchers also showed that MED1 acts directly to regulate estrogen signaling through a key pathway known to play a critical role in breast cancer. Testing of samples from human patients with breast cancer confirmed that MED1 is strongly correlated with HER2 cancer types.

"With these findings and our previously published study showing a tissue-specific role for MED1, we can now conduct further studies on MED1 as a disease-selective therapeutic target. Our team is currently using an RNA nanotechnology-based approach to select RNA aptamers (RNA molecules that bind to a specific target molecule) to specifically target MED1 LxxLL motifs to disrupt the MED1/estrogen receptor interactions to achieve this."



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