Exploring the Role of the TGF-β Signaling Pathway in Colorectal Precancerous Polyps Biochemical Genetics.

Abstract

Colorectal cancer (CRC) is an important public health issue and is the third most common cancer, accounting for approximately 10% of all cancer cases worldwide. CRC results from the accumulation of multiple genetic and epigenetic alterations in the normal epithelial cells of the colon and rectum, leading to the development of colorectal polyps and invasive carcinomas. The transforming growth factor-beta (TGF-β) pathway is regulated in many diseases, such as cancer. This factor can show tumor suppressant function in the early stages in healthy and cancer cells. It can be regulated and affected by different factors, including noncoding RNAs, which are the remarkable regulators for this pathway. The most prominent functions of this factor are cell cycle arrest and apoptosis in cancer cells. However, activating at the final stages of the cell cycle can cause tumor metastasis. Thus, the dual function of TGF-β and the pleiotropic nature of this signaling make it a crucial challenge for cancer treatment. Accurately studying the TGF-β signaling pathway is critical to determine its role. One of the roles of TGF-β signaling is its significant effect on colorectal polyp malignancy and cancer. In this article, we review the published scientific papers regarding the TGF-β signaling pathway, its related genes, and their contribution to precancerous conditions and colorectal cancer progression. The complex interaction of the TGF-β signaling pathway with noncoding RNAs, such as lncRNA TUG1 and miR-21, significantly influences colorectal polyp and cancer progression. Identifying dysregulated TGF-β-related noncoding RNAs offers promising therapeutic avenues for colorectal cancer. Comprehending TGF-β's connection to other molecular mechanisms is crucial for advancing effective therapeutic strategies.