Impact of MYC on metabolic reprogramming, cellular energetics, and tumorigenesis in Breast cancer

Abstract

Breast cancer is the most fatal malignancy reported in females. About 1.38 million cases of breast cancer were reported in 2022 among which 50% of breast cancer patients and around deaths of 60% had occurred in developing countries. A kind of transcription factor called MYC, encoded by the MYC oncogene, has a wide range of actions and an unexplained carcinogenic role. According to the available data, MYC initiates a gene amplification process through gene expression that fosters cell proliferation growth. A complex process of MYC to the uptake of nutrients to make ATP is also essential building blocks that increase cellular growth, activates DNA replication, and causes cell division. This is done through the help of its targets. In the field of translational cancer research shut down checkpoints and let MYC metabolic activities that support cell growth and proliferation loose. Unchecked growth related to dysregulated expression of MYC results in dependence on MYC-dependent metabolic pathways, and this dependence offers new targets for cancer therapy. Activity and expression of MYC are firmly upregulated in normal cells by several phenomena, as well as it depends on the stimulation of growth factor and overfull nutrient status. However, due to the dependence of MYC-driven tumors on already identified metabolic pathways, the synthetic lethal association between overexpression of MYC and certain enzymes gives inhibitors novel therapeutic opportunities. MYC is overexpressed in more than 50% of breast cancer patients, and its expression is connected with a very poor prognosis and a high risk of metastasis. MYC promotes breast cancer development and progression with several mechanisms, as well as the activation of cell proliferation, inhibition of apoptosis, and induction of angiogenesis. MYC also played a deciding role in the resistance to chemotherapy and radiation therapy.