Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer

Author:

Lee Yun Ju12ORCID,Kim Woo Ryung12,Park Eun Gyung12ORCID,Lee Du Hyeong12,Kim Jung-min12,Shin Hae Jin12,Jeong Hyeon-su12,Roh Hyun-Young23,Kim Heui-Soo23ORCID

Affiliation:

1. Department of Integrated Biological Sciences, Pusan National University, Busan 46241, Republic of Korea

2. Institute of Systems Biology, Pusan National University, Busan 46241, Republic of Korea

3. Department of Biological Sciences, College of Natural Sciences, Pusan National University, Busan 46241, Republic of Korea

Abstract

Colorectal cancer (CRC) is the third most prevalent cancer to be diagnosed, and it has a substantial mortality rate. Despite numerous studies being conducted on CRC, it remains a significant health concern. The disease-free survival rates notably decrease as CRC progresses, emphasizing the urgency for effective diagnostic and therapeutic approaches. CRC development is caused by environmental factors, which mostly lead to the disruption of signaling pathways. Among these pathways, the Wingless/Integrated (Wnt) signaling pathway, Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway, Mitogen-Activated Protein Kinase (MAPK) signaling pathway, Transforming Growth Factor-β (TGF-β) signaling pathway, and p53 signaling pathway are considered to be important. These signaling pathways are also regulated by non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). They have emerged as crucial regulators of gene expression in CRC by changing their expression levels. The altered expression patterns of these ncRNAs have been implicated in CRC progression and development, suggesting their potential as diagnostic and therapeutic targets. This review provides an overview of the five key signaling pathways and regulation of ncRNAs involved in CRC pathogenesis that are studied to identify promising avenues for diagnosis and treatment strategies.

Publisher

MDPI AG

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