Related Experiment Video
Updated: Jan 5, 2026
Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
MEG3 can affect the proliferation and migration of colorectal cancer cells through regulating miR-376/PRKD1 axis
Xiangbin Wu1, Jinlei Li1, Yuehan Ren1
1Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Wenzhou Medical University Wenzhou, Zhejiang, China.
Abstract:
The down-regulation of long non-coding RNA (lncRNA) MEG3 has been observed in various cancers; nonetheless, underlying mechanisms are still unclear. The current research work aims at exploring the roles of MEG3 in the pathogenesis of CRC and the associated mechanism. We observed that MEG3 was significantly down-regulated in both CRC tumor tissue and cell lines; also, the transient over-expression of MEG3 in CRC cell line SW480 and LoVo inhibited the proliferation and the migration and clone formation capability of cells; on the other hand, the knockdown of MEG3 has revealed opposite effects. Eventually, we figured it out that target miR-376 directly targeted both MEG3 and PRDK1 in SW480 and LoVo cells. To conclude, as our findings proved, MEG3 is likely to act as a tumor suppressor in the pathogenesis of CRC by means of the regulation of the miR-376/PRDK1 signal axis, suggesting that MEG3 has the potential to become a novel therapeutic target for the treatment of CRC.
Insights
Long non-coding RNA (lncRNA) MEG3 acts as a tumor suppressor in colorectal cancer (CRC). Its down-regulation promotes CRC progression by affecting the miR-376/PRDK1 signaling axis, indicating potential therapeutic applications.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Down-regulation of long non-coding RNA (lncRNA) MEG3 is implicated in various cancers, but its precise role and mechanisms in colorectal cancer (CRC) remain unclear.
- Understanding the function of MEG3 in CRC pathogenesis is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the role of MEG3 in the pathogenesis of colorectal cancer (CRC).
- To elucidate the underlying molecular mechanisms by which MEG3 influences CRC progression.
Main Methods:
- Quantitative analysis of MEG3 expression in CRC tumor tissues and cell lines.
- In vitro experiments involving transient over-expression and knockdown of MEG3 in CRC cell lines (SW480 and LoVo).
- Assessment of cell proliferation, migration, and clone formation capabilities.
- Identification of direct targets of MEG3 and its interaction with microRNA-376 (miR-376) and PRDK1.
Main Results:
- MEG3 expression was significantly down-regulated in CRC tissues and cell lines compared to normal controls.
- Over-expression of MEG3 inhibited proliferation, migration, and clone formation in CRC cells, while MEG3 knockdown promoted these processes.
- miR-376 was identified as a direct target of MEG3 and also targets PRDK1 in CRC cells.
Conclusions:
- MEG3 functions as a tumor suppressor in colorectal cancer (CRC).
- MEG3 exerts its tumor-suppressive effects by regulating the miR-376/PRDK1 signaling axis.
- MEG3 represents a potential novel therapeutic target for CRC treatment.
