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Triggering of Endoplasmic Reticulum Stress by Tannic Acid Inhibits the Proliferation and Migration of Colorectal
Fatemeh Shahabi Nejad1, Hadi Karami1,2, Maryam Darvish1
1Department of Molecular Medicine and Biotechnology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Introduction:
Due to the pivotal role of endoplasmic reticulum (ER) stress in cancers, interfering with its function can cause the accumulation of unfolded proteins, which ultimately leads to the activation of the unfolded protein response (UPR) signaling pathway and apoptosis. Therefore, the use of plant compounds such as tannic acid with UPR-inducing properties can be proposed as a possible treatment method for cancer. In this study, we investigated the effect of tannic acid on cell migration, colony formation, growth, and UPR-induced apoptosis in the SW48 colorectal cancer cell line.
Methods:
The MTT assay was performed to investigate the cytotoxic effect of tannic acid. We performed the qPCR method to elucidate the effect of tannic acid on the expression of Bim, MMP-9, Bcl-xL, cyclin D1, CHOP, and ATF4 genes. We also used the colony formation and migration experiments to investigate the effect of this compound on the colony formation and migration ability of tumor cells. Finally, we used Hoechst staining to measure cell apoptosis.
Results:
Tannic acid inhibited the cell survival, clonogenic, and migration of colon cancer cells. This compound increased the expression of ER stress-mediated UPR genes, ATF4 and CHOP. Moreover; tannic acid increased the expression of pro-apoptotic proteins like Bim, while at the same time causing a sharp decline in the expression of anti-apoptotic protein Bcl-xL. A decline in MMP-9 expression confirmed the anti-metastatic role of this compound.
Conclusion:
Taken together, tannic acid can induce apoptosis via ER stress-mediated UPR pathway, and has a suppressive effect on cell viability, growth, migration, colony formation, and metastasis, suggesting it may be a potential drug in colorectal cancer treatment.
Insights
Tannic acid, a plant compound, effectively inhibits colorectal cancer cell growth, migration, and metastasis by inducing apoptosis through the endoplasmic reticulum stress-mediated unfolded protein response (UPR) pathway. This suggests its potential as a novel cancer therapeutic.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Endoplasmic reticulum (ER) stress plays a critical role in cancer development.
- Interference with ER function triggers the unfolded protein response (UPR) and apoptosis.
- Plant-derived compounds like tannic acid show potential for cancer treatment due to UPR-inducing properties.
Purpose of the Study:
- To investigate the effects of tannic acid on colorectal cancer cells.
- To evaluate its impact on cell migration, colony formation, growth, and apoptosis.
- To explore its role in the UPR signaling pathway.
Main Methods:
- Cytotoxicity assessed using MTT assay.
- Gene expression analysis (Bim, MMP-9, Bcl-xL, cyclin D1, CHOP, ATF4) via qPCR.
- Colony formation and migration assays.
- Apoptosis measurement using Hoechst staining.
Main Results:
- Tannic acid suppressed cell viability, colony formation, and migration in SW48 colorectal cancer cells.
- Increased expression of ER stress-responsive genes (ATF4, CHOP) and pro-apoptotic protein Bim.
- Decreased expression of anti-apoptotic protein Bcl-xL and metastasis-associated gene MMP-9.
Conclusions:
- Tannic acid induces apoptosis via the ER stress-UPR pathway.
- It exhibits suppressive effects on colorectal cancer cell viability, growth, migration, and metastasis.
- Tannic acid demonstrates potential as a therapeutic agent for colorectal cancer.
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