Abstract
Every year, more than a million individuals are diagnosed with colorectal cancer (CRC) across the world. Certain lifestyle and genetic factors are known to drive the high incidence and mortality rates in some groups of individuals. The presence of enormous amounts of reactive oxygen species is implicated for the on-set and carcinogenesis, and oxidant scavengers are thought to be important in CRC therapy. In this review, we focus on the ethnicity-based CRC disparities in the U.S., the negative effects of oxidative stress and apoptosis, and gene regulation in CRC carcinogenesis. We also highlight the use of antioxidants for CRC treatment, along with screening for certain regulatory genetic elements and oxidative stress indicators as potential biomarkers to determine the CRC risk and progression.
Highlights
Emma Fernandez-Repollet, According to the World Health Organization, there were approximately 1.8 million new colorectal cancer (CRC) cases and around 861,000 deaths recorded in 2018 across the world [1]
Information-carrying biomolecules such as miRNAs, extracellular vesicles, circulating tumor cells, and cell-free DNA are known to regulate CRC metastasis through epithelial-mesenchymal transition, angiogenesis, immunosuppression, and chemoresistance [135,136,137,138,139,140,141,142]. Because of their importance in CRC carcinogenesis, these are considered potential biomarkers for disease progression and response to cancer therapies [135,136,137,138,139,140,141,142]. Though all of these have an excellent basis for use as genetic markers, due to their atypical expression patterns detected during CRC carcinogenesis, we focus on the roles of miRNAs in CRC progression and response to therapy [135,136]
Very few studies have been conducted to elucidate the molecular basis of CRC carcinogenesis in different ethnic groups
Summary
Emma Fernandez-Repollet, According to the World Health Organization, there were approximately 1.8 million new colorectal cancer (CRC) cases and around 861,000 deaths recorded in 2018 across the world [1]. The overaccumulation of reactive oxygen species (ROS) or reactive nitrogen species (RNS) in a cellular environment can damage the structure and function of the cells, leading to somatic mutation and neoplastic transformation [21] Both ROS and RNS are highly reactive and are formed in vivo via oxidation-reduction reactions. It is evident that CRC carcinogenesis is a complex process, in which cross-talks between environmental and lifestyle factors lead to the regulation of multiple molecular pathways for its occurrence. These intricate interactions may be the cause of resistance to drug or radiation-based therapies, implying a dire need for improved therapies to control one of the leading causes of cancer-based mortalities. We discuss how these pathways and regulatory genes, including some miRNAs, could be used as biomarkers or therapeutic targets for CRC
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