Illustration depicting E-cadherin acetylation unlocking cancer cell growth.

Unlocking Cancer's Code: How E-Cadherin Acetylation Fuels Tumor Growth

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Avery Sinclair in Health & Wellness December 2025 • 4 min read.

"New research reveals the surprising role of E-cadherin acetylation in colorectal cancer, offering potential targets for innovative therapies."


For years, scientists have understood that the E-cadherin protein is a crucial player in maintaining healthy tissues. Acting like cellular glue, E-cadherin helps cells stick together, forming strong barriers and preventing uncontrolled growth. However, recent studies have revealed a darker side to this protein, particularly when it comes to cancer. Instead of acting as a tumor suppressor, E-cadherin can sometimes promote tumor growth under specific conditions.

Emerging research indicates that changes in E-cadherin’s structure and location within the cell can dramatically alter its function. One such change is a process called acetylation, where a small chemical tag is added to the protein. While acetylation is a normal cellular process, in the context of E-cadherin, it seems to play a significant role in the development and progression of colorectal cancer.

This article dives into the groundbreaking research exploring how E-cadherin acetylation contributes to colorectal cancer. We will unpack the complex mechanisms behind this process, highlighting how it disrupts normal cell behavior and opens new avenues for potential cancer therapies. Get ready to delve into the cutting-edge science that could revolutionize our approach to fighting this deadly disease.

E-Cadherin's Double Life: From Tumor Suppressor to Promoter?

Illustration depicting E-cadherin acetylation unlocking cancer cell growth.

Normally, E-cadherin resides on the cell surface, where it binds to other E-cadherin molecules on neighboring cells. This creates strong connections that maintain tissue structure and prevent cells from detaching and spreading. Think of it like Velcro, holding everything in place. This function is crucial for preventing cancer cells from metastasizing or spreading to other parts of the body.

However, cancer cells are masters of disguise. In colorectal cancer, E-cadherin can be found inside the cell's nucleus. This relocation is not random; it's orchestrated by another protein called CTNND1. Once inside the nucleus, E-cadherin undergoes acetylation, a process that changes its function. This modification is facilitated by an enzyme called CREB-binding protein (CBP).

Here's what happens when E-cadherin is acetylated:
  • Its ability to bind to beta-catenin, another important protein, is weakened.
  • Beta-catenin is released and able to move freely in the nucleus.
  • This free beta-catenin then ramps up the expression of genes that promote tumor growth and migration.
This discovery is significant because it reveals a completely new way in which cancer cells can hijack normal cellular processes to fuel their growth. By modifying E-cadherin, cancer cells essentially flip its role, turning a tumor suppressor into a tumor promoter.

Targeting Acetylation: A New Hope for Colorectal Cancer Treatment?

The finding that E-cadherin acetylation promotes colorectal cancer growth opens up exciting possibilities for new therapies. Scientists are now exploring ways to block this process, effectively restoring E-cadherin’s tumor-suppressing function. One promising approach is to target the enzyme responsible for acetylation, CBP. By inhibiting CBP, we might be able to prevent E-cadherin from being modified, thus slowing down or even stopping tumor growth.

Another potential target is SIRT2, an enzyme that removes acetyl tags. By boosting SIRT2 activity, we could potentially reverse the acetylation of E-cadherin, shifting it back to its original role as a tumor suppressor. These strategies are still in the early stages of development, but they offer a glimmer of hope for more effective and targeted colorectal cancer treatments.

Further research is needed to fully understand the intricacies of E-cadherin acetylation and its role in cancer. However, this discovery marks a significant step forward in our fight against colorectal cancer. By unraveling the complex mechanisms that drive tumor growth, we can pave the way for innovative therapies that save lives.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1158/1541-7786.mcr-18-0637, Alternate LINK

Title: Nuclear E-Cadherin Acetylation Promotes Colorectal Tumorigenesis Via Enhancing Β-Catenin Activity

Subject: Cancer Research

Journal: Molecular Cancer Research

Publisher: American Association for Cancer Research (AACR)

Authors: Yongxu Zhao, Tao Yu, Nan Zhang, Jianxia Chen, Peng Zhang, Shuang Li, Lijun Luo, Zhenling Cui, Yue Qin, Feng Liu

Published: 2019-02-01

Everything You Need To Know

1

What is the role of E-cadherin in healthy tissues and how does it change in the context of cancer?

E-cadherin is a protein that normally acts as a tumor suppressor. It resides on the cell surface and helps cells stick together, maintaining tissue structure. In colorectal cancer, the function of E-cadherin can be altered. The article explains how E-cadherin's behavior can be hijacked by cancer cells.

2

What is acetylation and how does it affect E-cadherin?

Acetylation is a process where a small chemical tag is added to a protein. In the context of E-cadherin, this modification is facilitated by the enzyme CREB-binding protein (CBP). When E-cadherin undergoes acetylation, its ability to bind to beta-catenin is weakened. This allows beta-catenin to move freely in the nucleus, where it promotes tumor growth and migration. This modification is key in the context of colorectal cancer development and progression.

3

How does E-cadherin switch from being a tumor suppressor to a tumor promoter?

E-cadherin can sometimes promote tumor growth instead of suppressing it. When E-cadherin is found inside the cell's nucleus and undergoes acetylation, it loses its ability to bind to beta-catenin. This allows beta-catenin to promote tumor growth and migration. This change in function is a key element of colorectal cancer progression.

4

What is the role of CREB-binding protein (CBP) in this process?

The enzyme CREB-binding protein (CBP) is responsible for facilitating E-cadherin acetylation. Scientists are exploring ways to inhibit CBP to prevent E-cadherin from being modified. The goal is to restore E-cadherin’s tumor-suppressing function, and slow down or stop tumor growth in colorectal cancer.

5

What are the potential implications of this research for colorectal cancer treatment?

The discovery that E-cadherin acetylation promotes colorectal cancer growth opens up possibilities for new therapies. Targeting the enzyme CBP to block acetylation is a promising approach. By inhibiting CBP, scientists aim to prevent E-cadherin from being modified, potentially restoring its tumor-suppressing function. This could lead to new treatments for colorectal cancer.

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