Breast cancer is a heterogeneous disease and has complex mechanisms, which brings the need to come up with different approaches for its various types. Erbin is a member of the LAP family and directly interacts with ErbB2 (HER2), which is a crucial component for breast cancer sub-typing and treatment. Research on the relationship between Erbin and breast cancer showed different results since Erbin was seen to be able to act as both a tumor suppressor and a tumor promoter. There are multiple findings that Erbin has a role in the epithelial to mesenchymal transition in different cancer types. The role of Erbin in EMT is said to be multi-faceted, it affects multiple pathways that act on EMT progress. However, like Erbin’s contradictory role in breast cancer, there are different findings that support the conflicting claims on whether Erbin is an EMT promoter or not. These findings in the literature lead us to analyze how Erbin affects EMT in breast cancer. To investigate if there is a role of Erbin in EMT regulation, we have overexpressed Erbin in MCF7 and silenced Erbin in MDA-MB-231 with MDA-66 cell lines. With this experimental setup, we aimed to see how Erbin plays a role in EMT in both epithelial and mesenchymal cells as well as Luminal A, TNBC, and ER positive breast cancer types.
Our results showed that in TGFB induced EMT, Erbin levels are decreased in epithelial cells. Erbin overexpressed MCF7 cells show significant changes in the EMT markers compared to the control group. Experiments conducted with Erbin silenced MDA-MB-231 and MDA-66 cells also demonstrated significant changes in EMT marker levels. Our results suggest that Erbin has a role in EMT in breast cancer, and this role is not limited to one pathway and not streamlined, but possibly a big orchestration of different effects.