# ZFP161 promotes colorectal cancer progression by transcriptionally activating c-MYC

## TL;DR

ZFP161 promotes colorectal cancer by activating c-MYC, which increases cell growth and is linked to poor patient survival.

## Contribution

ZFP161 is identified as a direct transcriptional activator of c-MYC in human cells, linking it to cancer progression.

## Key findings

- ZFP161 binds to and activates the c-MYC promoter in human cells.
- High ZFP161 levels correlate with poor survival in colon adenocarcinoma patients.
- ZFP161 promotes tumorigenesis and malignant transformation of RPE-1 cells via c-MYC regulation.

## Abstract

Zinc Finger Protein 161 (ZFP161) is a key regulator of Ataxia Telangiectasia and Rad3-related (ATR) signaling, playing a crucial role in maintaining genomic stability. Human ZFP161 activates c-MYC, whereas its murine ortholog, ZF5, serves as a putative transcriptional repressor of c-MYC. In this study, we identified ZFP161 as a direct regulator of c-MYC. We show that ZFP161 binds to the promoter region of c-MYC, modulating its expression and downstream signaling pathways. Additionally, ZFP161 promotes cell proliferation and tumorigenesis through c-MYC regulation and contributes to the malignant transformation of non-cancerous retinal pigment epithelial (RPE-1) cells. Furthermore, high ZFP161 expression is associated with poor survival in patients with mixed colon adenocarcinoma. These findings suggest that the regulation of c-MYC by ZFP161 may represent a potential therapeutic target in c-MYC-driven cancers.