Abstract
Consumption of fruits and vegetables is associated with lower risk of several cancers, particularly colorectal cancer, which is mainly associated to their phytochemical content. A diverse range of phytochemicals, especially phenolic compounds, has been reported to possess important biological properties such as anticancer, antiviral, antioxidant and anti-inflammatory activities. Several factors contribute to the development of colorectal cancer. The scientific evidences support the genetic predisposition, diet, and lifestyle as some of the major contributing factors for colorectal cancer development. In this sense, this review aims to summarize the anticancer activities and the proposed mechanisms of action of phenolic acids with an emphasis in colon cancer through in vitro evidences. The evidences supports the theory of anticancer properties of phenolic acids, although the mechanisms are still not fully understood, but may include scavenging free radicals, induction of enzymes involved in the metabolism of xenobiotics, regulation of gene expression, modulation of cellular signaling pathways including those involved in DNA damage repair, cell proliferation, apoptosis and invasion.
Highlights
In the last few years, some studies have reported that the diet possesses an important role in the etiology of colorectal cancer
This mutational event is the initiating step in a pathway termed the adenoma-carcinoma sequence and involves genes such as APC (Adenomatous Polyposis Coli), K-ras, DCC (Deleted in Colorectal Cancer) and p53 (Figure 3), and is characterized by three stages: i.) initiation involving exposure to or uptake of carcinogens resulting in permanent DNA damage; ii.) Promotion involving a lengthy process of abnormal cell replication forming a preneoplastic lesion, and iii.) Progression of tumorigenesis involving gradual conversion of preneoplastic cells to malignant cells [2,8]
Role of phenolic acids on colon cancer A range of evidence supports the theory of anticancer properties of phenolic acids, the mechanisms are still not fully understood, but may include scavenging free radicals, induction of enzymes involved in the metabolism of xenobiotics, regulation of gene expression, modulation of cellular signaling pathways including those involved in DNA damage repair, cell proliferation, apoptosis and invasion
Summary
In the last few years, some studies have reported that the diet possesses an important role in the etiology of colorectal cancer. Development of CRC results from the accumulation of mutations or epigenetic changes that leads to transformation of normal colonic mucosa into colonic adenocarcinoma and subsequent carcinoma [7] This mutational event is the initiating step in a pathway termed the adenoma-carcinoma sequence and involves genes such as APC (Adenomatous Polyposis Coli), K-ras, DCC (Deleted in Colorectal Cancer) and p53 (Figure 3), and is characterized by three stages: i.) initiation involving exposure to or uptake of carcinogens resulting in permanent DNA damage; ii.) Promotion involving a lengthy process of abnormal cell replication forming a preneoplastic lesion, and iii.) Progression of tumorigenesis involving gradual conversion of preneoplastic cells to malignant cells [2,8]. The over-expression of inducible cyclooxygenases (COX-2), the enzyme which catalyzes a critical step in the conversion of arachidonic acid to prostaglandins and is induced by proinflammatory stimuli, including mitogens, cytokines and bacterial lipopolysaccharide (LPS), is believed to be associated with colon, lung, breast and prostate carcinogenesis [13]
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