Abstract illustration of LncRNA SNHG5 and microRNA-132-3p interaction in a colorectal cancer cell.

Decoding LncRNA SNHG5: A New Key to Colorectal Cancer?

Mira Elwood in Health & Wellness October 2025 • 4 min read.

"Unlocking the Role of LncRNA SNHG5 in Colorectal Cancer Progression: From Cell Growth to Metastasis"

Colorectal cancer (CRC) remains a significant global health challenge, ranking as one of the most prevalent cancer types worldwide. Despite advancements in diagnostic and therapeutic strategies, the complex molecular mechanisms driving CRC progression are not fully understood. This lack of understanding contributes to the persistently high mortality rates associated with advanced stages of the disease. Recent research has focused on the roles of non-coding RNAs, particularly long non-coding RNAs (lncRNAs), in cancer development and progression.

LncRNAs, characterized as RNA molecules longer than 200 nucleotides that do not code for proteins, have emerged as critical regulators of various biological processes, including cell growth, differentiation, and apoptosis. Aberrant expression of lncRNAs has been implicated in numerous cancers, highlighting their potential as therapeutic targets. Among these, LncRNA SNHG5 has garnered attention for its involvement in several types of cancer. However, its specific role and mechanism of action in colorectal cancer have remained elusive until now.

A recent study published in Cancer Biology & Therapy sheds light on the intricate role of LncRNA SNHG5 in colorectal cancer. The researchers investigated how SNHG5 affects cell proliferation, metastasis, and migration in CRC cells, focusing on its interactions with microRNA-132-3p (miR-132-3p) and CREB5, a protein involved in cell growth and survival. This article synthesizes the key findings of this research, providing a comprehensive overview of how SNHG5 influences CRC progression at the molecular level.

How Does LncRNA SNHG5 Influence Colorectal Cancer?

Abstract illustration of LncRNA SNHG5 and microRNA-132-3p interaction in a colorectal cancer cell.

The study begins by examining the expression levels of SNHG5, miR-132-3p, and CREB5 in both CRC tissues and cell lines. The researchers collected 25 pairs of CRC tissue samples alongside matched para-tumor tissues to measure the RNA and protein levels using quantitative real-time PCR (qRT-PCR) and Western blotting. These methods allowed them to quantify the gene expression and protein production in cancer cells compared to normal cells.

The study employed several advanced molecular biology techniques to explore the relationships between SNHG5, miR-132-3p, and CREB5:

qRT-PCR and Western Blotting: Used to quantify gene expression and protein levels.
Dual-Luciferase Reporter Assay: Confirmed direct interactions between miR-132-3p and SNHG5 or CREB5.
RNA Pull-Down Assay: Verified that SNHG5 directly binds to miR-132-3p.
CCK-8 Assay and Flow Cytometry: Assessed cell proliferation and apoptosis rates.
Transwell Assay and Scratch Test: Measured metastasis and migration capabilities of CRC cells.
In Vivo Experiments: Evaluated the effects of SNHG5 on CRC tumor growth in mice.

The researchers found that SNHG5 and CREB5 were significantly upregulated (increased) in CRC tissues and cells, while miR-132-3p was downregulated (decreased). Overexpression of SNHG5 and CREB5 promoted cell proliferation, metastasis, and migration, while inhibiting apoptosis (cell death). Conversely, increased expression of miR-132-3p had the opposite effect. These findings suggest that SNHG5 promotes CRC progression by suppressing miR-132-3p, which in turn, upregulates CREB5.

Future Implications and Therapeutic Potential

These findings highlight the importance of LncRNA SNHG5 as a potential therapeutic target in colorectal cancer. By understanding the molecular mechanisms through which SNHG5 promotes cancer progression, researchers can develop novel strategies to inhibit its activity. Future studies could focus on designing targeted therapies that disrupt the interaction between SNHG5 and miR-132-3p or that directly inhibit CREB5, offering new hope for patients with colorectal cancer.

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Everything You Need To Know

What is the significance of LncRNA SNHG5 in colorectal cancer, and how does it impact the disease's progression?

LncRNA SNHG5 has been identified as a pivotal factor in colorectal cancer (CRC) progression. The research indicates that increased levels of LncRNA SNHG5 are associated with enhanced cell proliferation, metastasis, and migration of CRC cells. These processes contribute to the spread and growth of cancer. LncRNA SNHG5 achieves these effects, in part, by suppressing miR-132-3p, which subsequently leads to the upregulation of CREB5, a protein that promotes cell survival and growth, thus fueling CRC progression.

How does miR-132-3p and CREB5 interact with LncRNA SNHG5, and what are the implications of these interactions in colorectal cancer?

In CRC, LncRNA SNHG5 interacts with miR-132-3p, acting as an inhibitor of this microRNA. This interaction leads to a reduction in miR-132-3p's activity. Consequently, with less miR-132-3p available, CREB5, a protein promoting cell growth and survival, is upregulated. The interplay among these three elements—SNHG5, miR-132-3p, and CREB5—is crucial. The upregulation of CREB5, due to the SNHG5's suppression of miR-132-3p, promotes CRC progression. This intricate molecular interplay highlights the importance of these molecules in the development and spread of CRC.

What experimental methods were used to study the role of LncRNA SNHG5 in colorectal cancer, and what did these methods reveal?

The study employed several advanced molecular biology techniques to investigate the impact of LncRNA SNHG5 in CRC. These methods included qRT-PCR and Western blotting to quantify gene expression and protein levels, dual-luciferase reporter assays and RNA pull-down assays to confirm the direct interactions between SNHG5, miR-132-3p and CREB5. Additionally, CCK-8 assays and flow cytometry assessed cell proliferation and apoptosis, while transwell assays and scratch tests measured metastasis and migration capabilities. In vivo experiments were also conducted to evaluate the effects of SNHG5 on CRC tumor growth in mice. These methods revealed that SNHG5 and CREB5 were upregulated in CRC tissues, while miR-132-3p was downregulated. Overexpression of SNHG5 and CREB5 promoted cell proliferation, metastasis, and migration, while increasing miR-132-3p expression had the opposite effects.

How might targeting LncRNA SNHG5 be used in the treatment of colorectal cancer?

The research suggests that LncRNA SNHG5 could be a potential therapeutic target. The identified mechanisms of action indicate that strategies to inhibit SNHG5's activity might slow or halt CRC progression. Possible approaches include developing therapies to disrupt the interaction between LncRNA SNHG5 and miR-132-3p, thereby restoring miR-132-3p's normal functions. Another strategy could involve directly inhibiting CREB5, the protein that SNHG5 indirectly activates. Such targeted therapies offer new hope for managing and treating CRC by addressing the root molecular causes of the disease.

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

This research has significant implications for the future of CRC treatment by shedding light on the complex molecular mechanisms driving CRC progression. The identification of LncRNA SNHG5 as a key player, along with its interactions with miR-132-3p and CREB5, provides a deeper understanding of the disease. This knowledge opens new avenues for developing targeted therapies aimed at disrupting these molecular pathways. The findings emphasize the potential of non-coding RNAs as therapeutic targets and pave the way for novel strategies that could improve patient outcomes and reduce mortality rates associated with CRC.