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New Protein Target Identified for Addressing Obesity-Linked Breast Cancer

New Protein Target Identified for Addressing Obesity-Linked Breast Cancer

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Scientists at the University of Kentucky have identified a protein called Hsp47 as a key driver of obesity-related breast cancer growth. Targeting this protein could lead to new treatments for patients with obesity-associated tumors.

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Researchers at the University of Kentucky Markey Cancer Center have uncovered a promising new target for treating breast cancer associated with obesity. The study, published in Breast Cancer Research, reveals that a protein called Hsp47 becomes more active in fat tissue during obesity, facilitating tumor growth by altering the tissue environment surrounding cancer cells.

The senior author, Dr. Ren Xu, explains that Hsp47 interacts with another protein, asporin, to stiffen the tissue matrix around tumors. This stiffening promotes cancer progression by creating a more conducive environment for tumor development. Under normal conditions, both proteins are maintained at balanced levels, but obesity causes Hsp47 levels to rise, leading to increased asporin secretion.

The team tested a drug named Col003, which inhibits Hsp47 activity. In mouse models fed high-fat diets, treatment with Col003 resulted in less weight gain and slower tumor growth compared to untreated mice. Notably, blocking Hsp47 also enhanced the presence of T-cells, immune cells responsible for attacking cancer, thereby boosting the body's natural defense mechanisms against tumors.

Obesity is a major health concern, particularly in Kentucky where nearly half of the population is classified as obese. Its link to increased cancer risk and poorer prognosis has been well established, and this new research provides insight into the molecular pathways involved. These findings suggest that targeting Hsp47 could be an effective strategy to mitigate obesity-related breast cancer progression.

Building on prior work, Dr. Xu's research previously identified Hsp47 as a factor in breast cancer metastasis, demonstrating its role in facilitating cancer cell spread by supporting interactions with blood platelets. The current findings add to this understanding by highlighting the protein’s involvement in obesity-driven tumor growth.

Overall, this discovery opens new avenues for developing therapies that specifically target the molecular consequences of obesity in breast cancer, potentially improving outcomes for patients affected by obesity and cancer.

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