Breast cancer is the most common cancer in women worldwide and remains a significant public health concern. Recent studies have shown that certain proteins in breast cancer cells can make them particularly aggressive and resistant to treatment. However, researchers have discovered a new approach to target these proteins and create an inhospitable environment for aggressive breast tumors. In this article, we will examine the use of protein inhibition as a potential therapeutic strategy and how it may impact the treatment of breast cancer.
Breast cancer is the second most common form of cancer in women in the United States, and most deaths related to this disease occur after it has metastasized beyond the breast. However, researchers led by Sarah Spiegel, PhD, at the Virginia Commonwealth University Massey Cancer Center recently discovered that the elimination of a protein called Sphingosine kinase 2 (SphK2) can significantly subdue breast cancer growth and spread. Specifically, the scientists determined that the deletion of SphK2 created a hostile environment for tumor cells that managed to halt the progression of triple-negative breast cancer and prevented it from spreading to the lungs. Triple-negative breast cancer is a highly aggressive form of the disease and, in the absence of actionable targets, exceedingly difficult to treat.
Spiegel and her team discovered that SphK2 is responsible for producing the lipid sphingosine-1-phosphate (S1P), a molecule known to play a role in the development of cancer, inflammation and cardiovascular disease. When they deleted SphK2 entirely, the tumor microenvironment (TME) was reprogrammed, which decreased the presence of S1P and increased the accumulation of the p53 tumor suppressor gene. The scientists believe that they have discovered a new and different approach to harness the p53 network that might pave the way for the development of a new class of therapeutics targeting SphK2 and the microenvironment that interferes with breast cancer progression and metastasis.
The findings of this preclinical experiment, published in Cancer Research, indicate that SphK2 inhibitors could be considered a multipronged treatment option to bolster clinical effectiveness in breast cancer. Spiegel emphasized, “The inability to effectively predict, prevent, and treat advanced breast cancer is a major problem in oncology care, and the development of additional effective targeted therapies is urgently required.”
Understanding the two-way communication that occurs between cancer cells and their microenvironment plays a direct role in breast cancer progression and spread, resistance to treatment, and overall patient outcome. Cancer growth changes the tumor microenvironment, necessitating a stronger comprehension of the cellular and molecular interplay driving the interactions between tumors and the surrounding tissue.
Spiegel collaborated on this study with researchers from VCU Massey Cancer Center and the University of Florida Health. This research can change the face of breast cancer treatment, especially triple-negative breast cancer that has been difficult to treat. More targeted therapy options could add value to patients’ lives and improve their chances of remission.
In conclusion, the discovery of protein inhibition as a potential treatment for aggressive breast tumors opens up the possibility of a new therapy option for individuals with this condition. The ability to target cancer cells specifically, without affecting the healthy cells, is a huge step forward in the field of cancer treatment. While further research is necessary to fully understand the implications of protein inhibition, the initial findings suggest that this could be a key strategy in the fight against breast cancer. We can hope that this research will continue to yield effective treatments and one day lead to a world where breast cancer is no longer a life-threatening disease.
