Researchers from Wenzhou Medical University in China have identified a mechanism involving long non-coding RNAs (lncRNA) that contributes to colorectal cancer (CRC) progression. CRC is the third most common cancer worldwide and is one of the most lethal cancers across the globe. Understanding the molecular mechanisms that underlie the development and progression of CRC is critical to developing biomarkers to detect it and new therapeutics to treat it. 

In the study, Fang et al. investigated the role of the lncRNA MIR3142HG in colorectal cancer. They also looked at the regulation of MIR3142HG by the IL-6/STAT3 signaling pathway. Previously, they had shown that thioredoxin-1 (Trx-1) interacts with STAT3 to promote CRC progression. Trx-1 is a small redox protein that can protect tumor cells during stress conditions. Translocation of IL-6 activated Trx-1 is an important role in CRC development, because this translocation activates the IL-6/STAT3 signaling pathway, which in turn promotes tumorigenesis. Working with this information, the researchers were able to identify MIR3142HG through RNA sequencing as a transcript that is regulated by IL-6 and Trx-1. 

Using CRC cell lines, they demonstrated that MIR3142HG overexpression enhanced proliferation and colony formation of CRC cells. Knockdown by antisense oligonucleotides (ASO) resulted in inhibited cell growth and colony formation. Further experiments in patient-derived organoids demonstrated that treatment with the MIR3142HG-ASOs inhibited growth as assessed by the CellTiter-Glo 2.0 Assay. Similar effects were seen with mouse xenografts. 

Furthermore, luciferase activity in the promoter constructs was quantified using the Dual-Luciferase® Reporter Assay System to evaluate STAT3-dependent transcriptional activation, and they identified a region of the reporter necessary for high transcriptional activity.  

When looking at samples from CRC tissues, they did note that low expression of MIR314HG was associated with advanced stage disease. To explain this paradoxical result, the authors posit that overexpression of this MIR3142HG may have one effect early in cancer development, such as promoting invasion and migration of cancer cells, but a different effect later during cancer progression that reduces cell survival in advanced tumors.  More data on mechanisms of action will be needed to fully understand these results.  

Literature Reviewed 

Fang, D. et al. (2025) IL-6-induced Long Noncoding RNA MIR3142HG Promotes Tumorigenesis by Interacting with Thioredoxin-1 and STAT-3 in Human Colorectal Cancer. Cell Mol Biol.  Lett. 30 (61) DOI: 10.1186/s11658-025-00742-6. 

The following two tabs change content below.

• Bio
• Latest Posts

Michele Arduengo

Supervisor, Digital Marketing Program Group at Promega Corporation

Michele earned her B.A. in biology at Wesleyan College in Macon, GA, and her PhD through the BCDB Program at Emory University in Atlanta, GA where she studied cell differentiation in the model system C. elegans. She taught on the faculty of Morningside University in Sioux City, IA, and continues to mentor science writers and teachers through volunteer activities. Michele manages the digital marketing program team at Promega.

Latest posts by Michele Arduengo (see all)

• IL-6/STAT3-Regulated Long Non-Coding RNA Is Involved in Colorectal Cancer Progression - July 1, 2025
• Using Dual-Luciferase Assays to Identify the Role of Non-Coding RNAs in Disease - May 2, 2025
• An Unexpected Role for RNA Methylation in Mitosis Leads to New Understanding of Neurodevelopmental Disorders - March 27, 2025