Akt Isoforms: A Family Affair in Breast Cancer

Simple Summary Breast cancer is the second leading cause of cancer-related death in women in the United States. The Akt signaling pathway is deregulated in approximately 70% of patients with breast cancer. While targeting Akt is an effective therapeutic strategy for the treatment of breast cancer, there are several members in the Akt family that play distinct roles in breast cancer. However, the function of Akt isoforms depends on many factors. This review analyzes current progress on the isoform-specific functions of Akt isoforms in breast cancer. Akt, also known as protein kinase B (PKB), belongs to the AGC family of protein kinases. It acts downstream of the phosphatidylinositol 3-kinase (PI3K) and regulates diverse cellular processes, including cell proliferation, cell survival, metabolism, tumor growth and metastasis. The PI3K/Akt signaling pathway is frequently deregulated in breast cancer and plays an important role in the development and progression of breast cancer. There are three closely related members in the Akt family, namely Akt1(PKB alpha), Akt2(PKB beta) and Akt3(PKB gamma). Although Akt isoforms share similar structures, they exhibit redundant, distinct as well as opposite functions. While the Akt signaling pathway is an important target for cancer therapy, an understanding of the isoform-specific function of Akt is critical to effectively target this pathway. However, our perception regarding how Akt isoforms contribute to the genesis and progression of breast cancer changes as we gain new knowledge. The purpose of this review article is to analyze current literatures on distinct functions of Akt isoforms in breast cancer.

Automated summary

This article discusses the importance of breast cancer in women in the United States and the role of Akt isoforms in the development of breast cancer. While Akt isoforms share similar structures, they exhibit redundant, distinct, and opposite functions in breast cancer. Understanding the isoform-specific function of Akt is critical for effectively targeting the Akt signaling pathway in cancer therapy.