Abstract
Cancer research has been heavily geared towards genomic events in the development and progression of cancer. In contrast, metabolic regulation, such as aberrant metabolism in cancer, is poorly understood. Alteration in cellular metabolism was once regarded simply as a consequence of cancer rather than as playing a primary role in cancer promotion and maintenance. Resurgence of cancer metabolism research has identified critical metabolic reprogramming events within biosynthetic and bioenergetic pathways needed to fulfill the requirements of cancer cell growth and maintenance. The tumor suppressor protein p53 is emerging as a key regulator of metabolic processes and metabolic reprogramming in cancer cells—balancing the pendulum between cell death and survival. This review provides an overview of the classical and emerging non-classical tumor suppressor roles of p53 in regulating mitochondrial dynamics: mitochondrial engagement in cell death processes in the prevention of cancer. On the other hand, we discuss p53 as a key metabolic switch in cellular function and survival. The focus is then on the conceivable roles of p53 in breast cancer metabolism. Understanding the metabolic functions of p53 within breast cancer metabolism will, in due course, reveal critical metabolic hotspots that cancers advantageously re-engineer for sustenance. Illustration of these events will pave the way for finding novel therapeutics that target cancer metabolism and serve to overcome the breast cancer burden.
Highlights
Nicknamed the “Guardian of the Genome,” p53 is believably the most extensively studied and most multifaceted tumor suppressor protein identified to date [1,2,3].The role of p53 extends well beyond its role as a tumor suppressor; it is emerging as an important regulator of metabolic homeostasis, pivotal in most major cellular processes [1,4,5,6,7,8]
Alongside its well-recognized role as a tumor suppressor, p53 has emerged as a major regulator of metabolic processes and metabolic programming and is intrinsically linked with mitochondria and mitochondrial dynamics associated with cell survival [1,15,16,17,45]
The studies highlighted in this review reveal that p53 has a plethora of functions in normal and cancer metabolism beyond the classical mitochondrial death syndrome
Summary
Nicknamed the “Guardian of the Genome,” p53 (encoded by the TP53 gene) is believably the most extensively studied and most multifaceted tumor suppressor protein identified to date [1,2,3]. The role of p53 extends well beyond its role as a tumor suppressor; it is emerging as an important regulator of metabolic homeostasis, pivotal in most major cellular processes [1,4,5,6,7,8]. Classical thinking supports that reinstating the p53 pathway may be one avenue of more efficacious breast cancer treatment through p53 activation of programmed cell death pathways. This concept may be flawed due to the poorly understood role of p53 in cellular metabolism, which is currently being widely revisited. We bring back the discussion to how these p53-reprogramming events may be important in cell survival and provide new avenues for breast cancer therapies
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