Published online Nov 15, 2023. doi: 10.4251/wjgo.v15.i11.1936
Peer-review started: April 19, 2023
First decision: June 20, 2023
Revised: June 29, 2023
Accepted: July 29, 2023
Article in press: July 29, 2023
Published online: November 15, 2023
Processing time: 210 Days and 3.8 Hours
Colorectal cancer (CRC) is one of the most prevalent and deadly types of cancer worldwide. Despite advances in treatment options, the molecular mechanisms underlying CRC development and progression are not fully understood. Recently, dopamine and cyclic adenosine monophosphate (cAMP)-regulated phosphoprotein with an apparent Mr of 32000 (DARPP-32) has emerged as a potential player in CRC. DARPP-32 is known for its involvement in dopamine and cAMP signaling pathways in the brain, but its role in CRC remains largely unexplored. Understanding the function and molecular mechanisms of DARPP-32 in CRC could provide valuable insights into the pathogenesis of this disease and potentially uncover new therapeutic targets.
CRC is a significant health concern, and understanding the underlying molecular mechanisms driving its progression is crucial for developing effective treatments. The role of DARPP-32, a protein involved in dopamine and cAMP signaling, in CRC remains poorly understood. Investigating the function of DARPP-32 in CRC could reveal its potential as a therapeutic target and shed light on novel pathways involved in tumor development and progression.
We aimed to enhance our understanding of the involvement of DARPP-32 in CRC progression and potentially identify novel therapeutic targets for the treatment of this disease.
Since the effect of DARPP-32 on colorectal neoplasia is unknown, this study combined bioinformatics analysis, quantitative polymerase chain reaction, western blotting, tissue microarrays, and a variety of in vitro and in vivo functional tests to investigate this effect.
We found that DARPP-32 was frequently upregulated in CRC and associated with abnormal clinicopathological features in CRC. Overexpression of DARPP-32 was shown to promote cancer progression. DARPP-32 knockdown resulted in the opposite functional effect. Mechanistically, DARPP-32 may regulate the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway to carry out its biological function.
The collective results demonstrate that DARPP-32 promotes CRC progression via the PI3K/AKT signaling pathway.
Further investigation is needed to reveal the precise molecular mechanisms through which DARPP-32 regulates the PI3K/AKT signaling pathway in CRC. Identifying the specific downstream targets and upstream regulators of DARPP-32 will provide a deeper understanding of its role in cancer progression.