期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms22010130
关键词
colorectal cancer; molecular pathways; chromosomal instability; microsatellite instability; therapeutics
资金
- Qatar University [QUHI-CMED-19/20-1, QUCG-CMED-20/21-2]
Colorectal cancer is the second leading cause of cancer-related mortality rates worldwide, with its prevalence still on the rise. Dysregulation of several cellular signaling pathways in CRC leads to malignant phenotypes. Studying signaling pathways helps elucidate the mechanisms of CRC progression and pharmacotherapy.
Colorectal cancer (CRC), the third most common type of cancer, is the second leading cause of cancer-related mortality rates worldwide. Although modern research was able to shed light on the pathogenesis of CRC and provide enhanced screening strategies, the prevalence of CRC is still on the rise. Studies showed several cellular signaling pathways dysregulated in CRC, leading to the onset of malignant phenotypes. Therefore, analyzing signaling pathways involved in CRC metastasis is necessary to elucidate the underlying mechanism of CRC progression and pharmacotherapy. This review focused on target genes as well as various cellular signaling pathways including Wnt/beta-catenin, p53, TGF-beta/SMAD, NF-kappa B, Notch, VEGF, and JAKs/STAT3, which are associated with CRC progression and metastasis. Additionally, alternations in methylation patterns in relation with signaling pathways involved in regulating various cellular mechanisms such as cell cycle, transcription, apoptosis, and angiogenesis as well as invasion and metastasis were also reviewed. To date, understanding the genomic and epigenomic instability has identified candidate biomarkers that are validated for routine clinical use in CRC management. Nevertheless, better understanding of the onset and progression of CRC can aid in the development of early detection molecular markers and risk stratification methods to improve the clinical care of CRC patients.
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