Related Experiment Video
Updated: Aug 6, 2026
Non-invasive Assessment of the Efficacy of New Therapeutics for Intestinal Pathologies Using Serial Endoscopic Imaging of Live Mice
Published on: March 10, 2015
Akkermansia muciniphila Aspartic Protease Amuc_1434* Inhibits Human Colorectal Cancer LS174T Cell Viability via
Xin Meng1, Jinrui Zhang1, Hao Wu2
1Key Laboratory for Molecular Enzymology and Engineering of Ministry of Education, College of Life Science, Jilin University, Changchun 130012, China.
Abstract:
Mucin2 (Muc2) is the main component of the intestinal mucosal layer and is highly expressed in mucous colorectal cancer. Previous studies conducted by our lab found that the recombinant protein Amuc_1434 (expressed in Escherichia coli prokaryote cell system, hereinafter termed Amuc_1434*), derived from Akkermansia muciniphila, can degrade Muc2. Thus, the main objective of this study was to explore the effects of Amuc_1434* on LS174T in colorectal cancer cells expressing Muc2. Results from this study demonstrated that Amuc_1434* inhibited the proliferation of LS174T cells, which was related to its ability to degrade Muc2. Amuc_1434* also blocked the G0/G1 phase of the cell cycle of LS174T cells and upregulated the expression of tumor protein 53 (p53), which is a cell cycle-related protein. In addition, Amuc_1434* promoted apoptosis of LS174T cells and increased mitochondrial ROS levels in LS174T cells. The mitochondrial membrane potential of LS174T cells was also downregulated by Amuc_1434*. Amuc_1434* can activate the death receptor pathway and mitochondrial pathway of apoptosis by upregulating tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL). In conclusion, our study was the first to demonstrate that the protein Amuc_1434* derived from Akkermansia muciniphila suppresses LS174T cell viability via TRAIL-mediated apoptosis pathway.
Insights
The Akkermansia muciniphila protein Amuc_1434* degrades Mucin2, inhibiting colorectal cancer cell proliferation. This protein induces apoptosis and cell cycle arrest in LS174T cells via the TRAIL pathway.
Area of Science:
- Microbiology
- Molecular Biology
- Cancer Research
Background:
- Mucin2 (Muc2) is a key component of the intestinal mucus layer and is overexpressed in colorectal cancer.
- The recombinant protein Amuc_1434*, derived from Akkermansia muciniphila, has been shown to degrade Muc2.
Purpose of the Study:
- To investigate the effects of Amuc_1434* on LS174T colorectal cancer cells that express Muc2.
- To elucidate the mechanisms underlying Amuc_1434*'s impact on cancer cell viability.
Main Methods:
- Treatment of LS174T cells with Amuc_1434*
- Analysis of cell proliferation, cell cycle phase, apoptosis, mitochondrial reactive oxygen species (ROS) levels, and mitochondrial membrane potential.
- Assessment of tumor protein 53 (p53) and tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL) expression.
Main Results:
- Amuc_1434* significantly inhibited LS174T cell proliferation by degrading Muc2.
- Amuc_1434* induced G0/G1 cell cycle arrest and upregulated p53 expression.
- Amuc_1434* promoted apoptosis through both death receptor and mitochondrial pathways, evidenced by increased ROS, decreased mitochondrial membrane potential, and upregulated TRAIL.
Conclusions:
- The study demonstrates that Amuc_1434* suppresses LS174T cell viability.
- Amuc_1434* acts via Muc2 degradation, cell cycle arrest, and TRAIL-mediated apoptosis.
- This research highlights Amuc_1434* as a potential therapeutic agent for colorectal cancer.
