Apoptosis Mechanisms: Role of Anti-apoptotic Proteins, Cancer Hallmarks and Tumor Microenvironment in Cancer Cell Survival

Abstract

Apoptosis, or programmed cell death, is the result of signaling pathways being activated when cells experience irreversible alterations due to internal or external stress. To stop cancer from developing, this procedure is crucial for getting rid of potentially dangerous cells that have accumulated genetic damage. Nevertheless, a lot of cancer cells create defenses against death, which aids in the growth of tumors and treatment resistance. Certain intracellular proteins play a key role in blocking apoptosis by interfering with specific stages of the cell death process. Among these, members of the Bcl-2 family such as Bcl-2 and Bcl-xL help maintain the integrity of cellular membranes, including those of the plasma membrane, endoplasmic reticulum, and mitochondria. Additionally, Bcl-2 is believed to exhibit inherent antioxidant properties. The transition from normal cells to malignant tumors involves the acquisition of distinct functional traits, often referred to as the hallmarks of cancer. The tumor microenvironment (TME) plays a critical role in this transformation, facilitating tumor growth by providing essential nutrients and interacting dynamically with cancer cells. This paper focuses on the role of Inhibitor of Apoptosis Proteins (IAPs) and anti-apoptotic proteins like Bcl-2, both of which contribute to cancer progression by preventing cell death. Their ability to enhance cell survival promotes tumor growth and resistance to treatment. Additionally, the review underscores the TME's significance, including the microbiome's influence in modulating apoptosis and shaping tumor behavior. Targeting elements of the TME could improve therapeutic strategies and enhance treatment efficacy.