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Updated: Oct 3, 2025

In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
VSNL1 Promotes Cell Proliferation, Migration, and Invasion in Colorectal Cancer by Binding with COL10A1
Chuan He1, Weiguo Liu1, Yan Xiong1
1Department of Digestive Oncology, Medical College of Nanchang University, Cancer Hospital of Jiangxi Province, Nanchang, Jiangxi, China.
Objective:
The study aimed to explore the role of VSNL1/COL10A1 axis in colorectal cancer.
Methods:
The differential-expressed mRNA in colorectal cancer tissues and adjacent tissues were analyzed through GEO database and GEPIA database. The target genes of mRNA were predicted through the Starbase database, and the targeting relationship of mRNA was verified by co-IP assay. The expressions of VSNL1 and COL10A1 were detected by RT-PCR and immunohistochemistry. Cell viability and proliferation were detected by CCK8 assay and EdU assay, respectively. Cell migration and invasion were detected by transwell assay. The expression of related proteins was detected by western blot.
Results:
VSNL1 was significantly overexpressed in colorectal cancer tissues compared with adjacent tissues. In addition, downregulation of VSNL1 could inhibit the proliferation, migration, and invasion of colorectal cancer cells. The co-IP experiment indicated that VSNL1 could bind with COL10A1. Further studies demonstrated that upregulation of COL10A1 could promote colorectal cells proliferation, migration, invasion, and reverse the effect of sh-VSNL1 on colorectal cancer cells.
Conclusion:
VSNL1 could promote the proliferation, migration, and invasion of colorectal cancer by targeting COL10A1. VSNL1 might be a potential target for colorectal cancer treatment.
Insights
Visinin-like protein 1 (VSNL1) promotes colorectal cancer growth by targeting Collagen Type X Alpha 1 (COL10A1). Targeting this VSNL1/COL10A1 axis may offer new colorectal cancer treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Colorectal cancer (CRC) remains a significant global health challenge.
- Understanding the molecular mechanisms driving CRC progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the functional role of the VSNL1/COL10A1 axis in colorectal cancer.
- To explore VSNL1 and COL10A1 as potential therapeutic targets for CRC.
Main Methods:
- Bioinformatic analysis of GEO and GEPIA databases for differential gene expression.
- In vitro assays including cell viability (CCK8), proliferation (EdU), migration, and invasion (Transwell).
- Molecular techniques such as co-immunoprecipitation (co-IP), RT-PCR, immunohistochemistry, and Western blot.
Main Results:
- VSNL1 was significantly overexpressed in colorectal cancer tissues.
- Downregulation of VSNL1 inhibited cancer cell proliferation, migration, and invasion.
- VSNL1 physically interacted with COL10A1, and COL10A1 upregulation promoted CRC cell growth, reversing VSNL1 knockdown effects.
Conclusions:
- The VSNL1/COL10A1 axis promotes colorectal cancer progression.
- VSNL1 acts through COL10A1 to enhance proliferation, migration, and invasion.
- This axis represents a promising therapeutic target for colorectal cancer treatment.
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