DNA transforming into healthy colon

Unlocking the Code: How LncRNA SNHG5 Could Revolutionize Colorectal Cancer Treatment

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Beau Callahan in Health & Wellness December 2025 • 4 min read.

"New research unveils the crucial role of a long non-coding RNA in colorectal cancer, offering potential for innovative therapies."


Colorectal cancer (CRC) remains a significant global health challenge, ranking as the second most common cancer in women and the third in men. Despite advancements in prevention, diagnosis, and treatment, the overall survival rate for CRC patients remains unsatisfactory. This is largely due to the intricate and often elusive molecular mechanisms that drive the disease. Recent research is shedding light on these mechanisms, offering hope for more effective therapies.

Long non-coding RNAs (lncRNAs) have emerged as key players in various biological processes, including cancer development. One such lncRNA, SNHG5, has been implicated in numerous cancers, but its specific role in colorectal cancer has remained unclear. A groundbreaking study has now uncovered how SNHG5 affects cell proliferation, metastasis, and migration in CRC, paving the way for potential therapeutic interventions.

This article explores the findings of this pivotal study, detailing how SNHG5 interacts with other molecules to fuel the progression of colorectal cancer. By understanding these intricate relationships, scientists hope to develop targeted treatments that can significantly improve outcomes for CRC patients.

The SNHG5-miR-132-3p-CREB5 Pathway: A Deep Dive into Colorectal Cancer Development

DNA transforming into healthy colon

The study's core discovery revolves around the SNHG5-miR-132-3p-CREB5 pathway. Researchers found that SNHG5 acts as a molecular sponge, soaking up miR-132-3p. MiR-132-3p is a microRNA that typically suppresses tumor growth. By binding to miR-132-3p, SNHG5 effectively neutralizes its tumor-suppressing activity. This, in turn, allows CREB5 (cAMP Responsive Element Binding Protein 5), a protein that promotes cell proliferation and survival, to become more active.

In essence, SNHG5 promotes cancer cell growth and spread by inhibiting a tumor suppressor (miR-132-3p) and activating a cell growth promoter (CREB5). This intricate interplay highlights the complexity of molecular events driving colorectal cancer.

Here’s a breakdown of the key findings:
  • SNHG5 is Upregulated in CRC: CRC tissues showed significantly higher levels of SNHG5 compared to adjacent normal tissues.
  • SNHG5 Promotes Cell Proliferation: Overexpression of SNHG5 led to increased proliferation, migration, and metastasis of CRC cells.
  • SNHG5 Inhibits Apoptosis: Higher SNHG5 levels were associated with a decrease in programmed cell death (apoptosis) in CRC cells.
  • MiR-132-3p is Downregulated: CRC tissues exhibited lower levels of miR-132-3p compared to normal tissues.
  • CREB5 is Upregulated: CRC tissues showed higher levels of CREB5, further driving cancer progression.
These findings were further validated through in vivo experiments, where silencing SNHG5 significantly inhibited tumor growth in mice. This underscores the therapeutic potential of targeting SNHG5 in colorectal cancer treatment.

The Future of Colorectal Cancer Treatment: Targeting SNHG5

This research marks a significant step forward in our understanding of the molecular mechanisms driving colorectal cancer. By identifying SNHG5 as a key regulator of cell proliferation, metastasis, and apoptosis, scientists have opened new avenues for therapeutic intervention. Future research will focus on developing strategies to target SNHG5, potentially through RNA interference or other gene-silencing techniques. Such targeted therapies could offer a more effective and less toxic approach to treating colorectal cancer, ultimately improving outcomes for patients worldwide.

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.

Everything You Need To Know

1

What is LncRNA SNHG5, and what role does it play in colorectal cancer?

LncRNA SNHG5 is a long non-coding RNA that has been found to be present in higher amounts in colorectal cancer tissues compared to normal tissues. It acts as a molecular sponge, soaking up miR-132-3p, which is a microRNA that typically suppresses tumor growth. By neutralizing miR-132-3p's tumor-suppressing activity, SNHG5 allows CREB5, a protein that promotes cell proliferation and survival, to become more active. This entire mechanism contributes to cancer cell growth and spread.

2

Why is the SNHG5-miR-132-3p-CREB5 pathway important in understanding colorectal cancer?

The SNHG5-miR-132-3p-CREB5 pathway is significant because it highlights a critical molecular mechanism driving colorectal cancer development. SNHG5, by inhibiting miR-132-3p and activating CREB5, promotes cancer cell proliferation, migration, and metastasis. This pathway offers potential targets for therapeutic intervention, such as silencing SNHG5 to inhibit tumor growth.

3

What is the function of MiR-132-3p, and how is it affected in colorectal cancer?

MiR-132-3p is a microRNA that usually functions to suppress tumor growth. In colorectal cancer, miR-132-3p is downregulated, meaning it is present in lower levels compared to normal tissues. This reduction in miR-132-3p allows cancer cells to grow and spread more easily. Understanding the role of miR-132-3p and how SNHG5 interacts with it provides insights into potential therapeutic strategies.

4

Can you explain what CREB5 is and how it contributes to the development of colorectal cancer?

CREB5, or cAMP Responsive Element Binding Protein 5, is a protein that promotes cell proliferation and survival. In colorectal cancer, CREB5 is found to be upregulated, meaning it is present in higher levels, which further drives cancer progression. This protein is activated due to SNHG5 inhibiting the function of miR-132-3p. Targeting CREB5, or the pathway leading to its activation, represents a potential avenue for treatment.

5

How might targeting SNHG5 change the way colorectal cancer is treated in the future?

Targeting SNHG5 could revolutionize colorectal cancer treatment by addressing a key regulator of cell proliferation, metastasis, and apoptosis. Strategies like RNA interference or other gene-silencing techniques could be used to reduce SNHG5 levels, thereby inhibiting tumor growth and improving patient outcomes. Unlike traditional treatments, this approach has the potential to be more targeted and less toxic.

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