Breast Cancer Coverage from Every Angle

Heat Shock Protein 47 and Breast Cancer Metastasis

By: Julia Fiederlein
Posted: Tuesday, March 31, 2020

Increased expression of a protein involved in the production of collagen known as heat shock protein 47 (Hsp47) appears to be associated with the metastasis of breast cancer, according to Ren Xu, PhD, of the University of Kentucky Markey Cancer Center, Lexington, and colleagues. Results of the study, which were published in PNAS, may shed light on the mesenchymal phenotypes in cancer cells and how they contribute to the spread of breast cancer.

“Targeting Hsp47 could be a promising strategy to block cancer cell–platelet interaction and cancer colonization in secondary organs for triple-negative breast cancer patients,” Dr. Xu stated in a University of Kentucky press release.

In brief, epithelial-mesenchymal transition is the event in which cells lose their epithelial qualities to become migrating mesenchymal cells. This cellular event is crucial for metastasis, as it promotes the migration of cancer cells and allows them to invade and colonize other organs. The binding of the cancer cell to a platelet allows for increased survival during this process. Previous studies have found that type I collagen seems to play a role in promoting epithelial-mesenchymal transition, and high levels of collagen deposition and expression are associated with metastasis and poor prognosis in patients with breast cancer.

The team of investigators conducted in vivo xenograft experiments using 6-week-old female SCID mice, fluorescence-activated cell sorting of platelet recruitment using mouse platelets, clustering assays, and transendothelial migration assays to examine the role of the Hsp47 protein in the metastasis of breast cancer. It was found that expression of both Hsp47 and collagen expression is induced during the epithelial-mesenchymal transition process. The increased expression of Hsp47 was determined to promote cancer cell–platelet interactions through the induction of collagen deposition, allowing for the clustering of cancer cells and invasion of distant organs. The researchers identified the Hsp47/collagen axis as the regulator of cancer cell–platelet interactions and, therefore, metastasis.

“If we can find a way to target this pathway with therapeutics, we could block this process and therefore inhibit metastasis,” Dr. Xu commented.

Disclosure: The study authors reported no conflicts of interest.

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