# Prkci acts a pro-proliferation factor in colorectal cancer

## TL;DR

This study shows that Prkci promotes colorectal cancer growth by stabilizing c-Myc, suggesting it could be a new target for treatment.

## Contribution

The study identifies Prkci as a novel pro-proliferation factor in CRC through its stabilization of c-Myc via phosphorylation.

## Key findings

- Prkci is overexpressed in CRC and linked to poor prognosis.
- Prkci knockout reduces tumor growth in vitro and in vivo.
- Prkci stabilizes c-Myc by phosphorylating serine 21, preventing its degradation.

## Abstract

Colorectal cancer (CRC) is a common malignancy with high mortality, and its treatment remains challenging in advanced stages. Protein kinase C iota (Prkci), a member of the atypical PKC family, is implicated in several cancers, yet its role in CRC is unclear. Here, we report that Prkci is overexpressed in CRC and correlates with poor prognosis. Functional assays showed that Prkci enhances proliferation and metabolic activity, while its knockout suppresses tumor growth both in vitro and in vivo. Mechanistically, Prkci interacts with and phosphorylates c-Myc at serine 21, thereby inhibiting its ubiquitin-mediated degradation and stabilizing the protein. The pro-proliferative effect of Prkci is dependent on c-Myc S21 phosphorylation. In mouse models, deletion of Prkci significantly delayed tumor growth and improved survival. These findings identify Prkci as a key regulator of CRC progression via post-translational stabilization of c-Myc, highlighting it as a potential therapeutic target in colorectal cancer.