Surreal illustration of interconnected nodes in cancerous and healthy colon tissue.

Cracking the Code: How a Tiny Loop Could Revolutionize Colorectal Cancer Treatment

Jordan Keane in Health & Wellness November 2025 • 3 min read.

"Scientists Discover a Key Feedback Loop in Colorectal Cancer Development, Offering New Avenues for Targeted Therapies"

Colorectal cancer (CRC) remains a significant health challenge worldwide. While treatments have improved, the need for more effective and targeted therapies is ever-present. Recent research has shed light on a fascinating feedback loop within cancer cells that could pave the way for new treatment approaches.

A team of scientists has identified a critical link between several key proteins within colorectal cancer cells: c-MYC, NAMPT, and SIRT1. This loop appears to be activated in the early stages of both major pathways leading to CRC, offering a potential target for intervention.

This article explores the details of this discovery, explaining the role of each protein and how their interaction contributes to cancer development. We'll also delve into the potential therapeutic implications, including the possibility of developing drugs that specifically target this feedback loop.

The c-MYC/NAMPT/SIRT1 Loop: What is it and Why Does it Matter?

Surreal illustration of interconnected nodes in cancerous and healthy colon tissue.

At the heart of this discovery lies a positive feedback loop involving three key proteins: c-MYC, NAMPT, and SIRT1. Understanding the function of each is crucial to grasping the significance of the loop:

Let's break down the roles and interaction:

c-MYC: This is a well-known proto-oncogene, meaning it has the potential to cause cancer when it is abnormally activated. It regulates cell growth, proliferation, and metabolism.
NAMPT (Nicotinamide Phosphoribosyltransferase): An enzyme crucial for producing NAD+, a vital molecule for cellular energy and function. NAMPT is also implicated in cancer development and progression.
SIRT1 (Silent Information Regulator 1): A protein deacetylase involved in various cellular processes, including stress resistance, DNA repair, and metabolism. SIRT1 has been shown to promote cancer cell survival.

The study reveals that c-MYC increases the levels of NAMPT, which leads to higher NAD+ production and, consequently, increased SIRT1 activity. SIRT1, in turn, further enhances c-MYC activity, creating a self-amplifying loop that fuels cancer cell growth and survival.

A Promising Future for Colorectal Cancer Therapy

This study's findings offer a compelling rationale for exploring therapies that target the c-MYC/NAMPT/SIRT1 feedback loop. By inhibiting NAMPT or SIRT1, it may be possible to disrupt this loop, suppress cancer cell growth, and improve treatment outcomes, especially in the serrated subtype of colorectal cancer.

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: 10.1007/s12032-018-1225-1, Alternate LINK

Title: The C-Myc/Nampt/Sirt1 Feedback Loop Is Activated In Early Classical And Serrated Route Colorectal Cancer And Represents A Therapeutic Target

Subject: Cancer Research

Journal: Medical Oncology

Publisher: Springer Science and Business Media LLC

Authors: Lydia Brandl, Nina Kirstein, Jens Neumann, Andrea Sendelhofert, Michael Vieth, Thomas Kirchner, Antje Menssen

Published: 2018-11-20

Everything You Need To Know

What is the c-MYC/NAMPT/SIRT1 feedback loop, and why is it important in the context of colorectal cancer?

The research identifies a positive feedback loop involving c-MYC, NAMPT, and SIRT1. Specifically, c-MYC elevates NAMPT levels, boosting NAD+ production and subsequently enhancing SIRT1 activity. SIRT1 then amplifies c-MYC activity, establishing a self-perpetuating cycle that promotes cancer cell growth and survival. This loop is significant because it is activated in the early stages of colorectal cancer development, making it a potential target for therapeutic intervention.

Can you explain the individual roles of c-MYC, NAMPT, and SIRT1 within the identified feedback loop?

c-MYC is a proto-oncogene involved in cell growth, proliferation, and metabolism. NAMPT, or Nicotinamide Phosphoribosyltransferase, is an enzyme that produces NAD+, essential for cellular energy and function and also implicated in cancer progression. SIRT1, or Silent Information Regulator 1, is a protein deacetylase involved in stress resistance, DNA repair, and metabolism, promoting cancer cell survival. Together, they form a loop where each protein enhances the activity or production of the others, driving cancer development.

How could targeting NAMPT or SIRT1 potentially lead to new colorectal cancer therapies?

Targeting NAMPT or SIRT1 could disrupt the c-MYC/NAMPT/SIRT1 feedback loop. Inhibiting NAMPT would reduce NAD+ production, limiting SIRT1 activity. Similarly, inhibiting SIRT1 directly would prevent it from further enhancing c-MYC activity. Breaking this loop could suppress cancer cell growth and improve treatment outcomes, especially in specific colorectal cancer subtypes like the serrated subtype. This strategy focuses on starving the cancer cells by disrupting their energy and growth pathways.

What are the limitations of the study's findings, and what areas require further research to translate these discoveries into clinical applications?

The study doesn't delve into the specifics of drug development or clinical trials. It also doesn't explore the potential side effects of targeting NAMPT or SIRT1, or how these therapies might interact with existing cancer treatments. Further research is needed to understand the long-term effects and optimal strategies for targeting this loop in different patient populations and cancer stages. It's important to know if inhibiting NAMPT or SIRT1 would have adverse effects on healthy cells.

Besides the c-MYC/NAMPT/SIRT1 loop, what other factors contribute to colorectal cancer development, and how might they interact with this loop?

While the study highlights the c-MYC/NAMPT/SIRT1 loop, other signaling pathways and genetic mutations also contribute to colorectal cancer. For instance, mutations in genes like APC, KRAS, and TP53 are known drivers of CRC. The interplay between these factors and the c-MYC/NAMPT/SIRT1 loop is complex. Future research should investigate how these pathways interact and whether targeting the c-MYC/NAMPT/SIRT1 loop can synergize with other therapeutic approaches that address these additional genetic and molecular drivers of CRC. Also immune evasion could be at play and isn't discussed in this context.