Bibliographic Details
Title: |
RNA Binding Proteins as Potential Therapeutic Targets in Colorectal Cancer. |
Authors: |
Singh, Vikash, Singh, Amandeep, Liu, Alvin John, Fuchs, Serge Y., Sharma, Arun K., Spiegelman, Vladimir S. |
Source: |
Cancers; Oct2024, Vol. 16 Issue 20, p3502, 26p |
Subject Terms: |
THERAPEUTIC use of antineoplastic agents, RNA-binding proteins, CANCER invasiveness, DRUG resistance in cancer cells, HOMEOSTASIS, COLORECTAL cancer, GENE expression, METASTASIS, MESSENGER RNA, TUMOR suppressor genes, SMALL molecules, ONCOGENES, MOLECULAR structure, DISEASE progression, DRUG discovery, CHEMICAL inhibitors |
Abstract: |
Simple Summary: RNA-binding proteins (RBPs) are crucial in regulating gene expression in the intestine, and their abnormal activity can lead to colorectal cancer (CRC). This review explores how specific RBPs, such as LIN28, IGF2BPs, Musashi, HuR, and CELF1, contribute to CRC by affecting the stability and translation of key cancer-related genes. These proteins can promote tumor growth, spread, and resistance to treatments. Although targeting RBPs is challenging, recently discovered small molecules can disrupt the harmful interactions, showing promise for new CRC therapies. Further research and development of RBP-targeting agents should lead to better treatment options for CRC patients. RNA-binding proteins (RBPs) play critical roles in regulating post-transcriptional gene expression, managing processes such as mRNA splicing, stability, and translation. In normal intestine, RBPs maintain the tissue homeostasis, but when dysregulated, they can drive colorectal cancer (CRC) development and progression. Understanding the molecular mechanisms behind CRC is vital for developing novel therapeutic strategies, and RBPs are emerging as key players in this area. This review highlights the roles of several RBPs, including LIN28, IGF2BP1–3, Musashi, HuR, and CELF1, in CRC. These RBPs regulate key oncogenes and tumor suppressor genes by influencing mRNA stability and translation. While targeting RBPs poses challenges due to their complex interactions with mRNAs, recent advances in drug discovery have identified small molecule inhibitors that disrupt these interactions. These inhibitors, which target LIN28, IGF2BPs, Musashi, CELF1, and HuR, have shown promising results in preclinical studies. Their ability to modulate RBP activity presents a new therapeutic avenue for treating CRC. In conclusion, RBPs offer significant potential as therapeutic targets in CRC. Although technical challenges remain, ongoing research into the molecular mechanisms of RBPs and the development of selective, potent, and bioavailable inhibitors should lead to more effective treatments and improved outcomes in CRC. [ABSTRACT FROM AUTHOR] |
|
Copyright of Cancers is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
Database: |
Complementary Index |
Full text is not displayed to guests. |
Login for full access.
|