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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
JianPi JieDu Recipe Inhibits Epithelial-to-Mesenchymal Transition in Colorectal Cancer through TGF-β/Smad Mediated
Xuan Liu1, Qing Ji1, Wanli Deng1
1Department of Medical Oncology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, 528 Zhangheng Road, Shanghai 201203, China.
Abstract:
JPJD was an ideal alternative traditional Chinese medicine compound in the prevention and treatment of CRC, but its underlying mechanisms has not been fully elucidated. In this study, we demonstrated in vitro that TGF-β-induced EMT promoted the invasion and metastasis of CRC cells, reduced the expression of E-cadherin, and elevated the expression of Vimentin. However, JPJD could inhibit the invasive and migratory ability of TGF-β-stimulated CRC cells in a concentration-dependent manner through increasing the expression of E-cadherin and repressing the expression of Vimentin, as well as the inhibition of TGF-β/Smad signaling pathway. Meanwhile, JPJD reduced the transcriptional activities of EMT-associated factors Snail and E-cadherin during the initiation of TGF-β-induced EMT. In vivo, the results demonstrated that JPJD can significantly inhibit the liver and lung metastasis of orthotopic CRC tumor in nude mice, as well as significantly prolonging the survival time of tumor-bearing in a dose-dependent manner. Additionally, JPJD can upregulate the expression of E-cadherin and Smad2/3 in the cytoplasm and downregulate the expression of Vimentin, p-Smad2/3, and Snail in the orthotopic CRC tumor tissues. In conclusions, our new findings provided evidence that JPJD could inhibit TGF-β-induced EMT in CRC through TGF-β/Smad mediated Snail/E-cadherin expression.
Insights
JPJD, a traditional Chinese medicine, inhibits colorectal cancer (CRC) cell invasion and metastasis by blocking TGF-β-induced epithelial-mesenchymal transition (EMT). This compound enhances E-cadherin and reduces Vimentin, offering a promising therapeutic strategy for CRC.
Area of Science:
- Oncology
- Traditional Chinese Medicine
- Molecular Biology
Background:
- Colorectal cancer (CRC) metastasis is a significant challenge.
- Epithelial-mesenchymal transition (EMT) is crucial for cancer cell invasion and metastasis.
- The precise mechanisms of traditional Chinese medicine (TCM) compounds like JPJD in CRC remain unclear.
Purpose of the Study:
- To elucidate the underlying mechanisms of JPJD in inhibiting TGF-β-induced EMT in CRC.
- To evaluate the in vitro and in vivo efficacy of JPJD against CRC cell invasion and metastasis.
- To investigate the impact of JPJD on the TGF-β/Smad signaling pathway and EMT-associated factors.
Main Methods:
- In vitro studies using CRC cells to assess cell invasion, migration, and expression of EMT markers (E-cadherin, Vimentin).
- In vivo experiments using orthotopic CRC tumor models in nude mice to evaluate metastasis inhibition and survival rates.
- Analysis of TGF-β/Smad signaling pathway components and EMT-related transcription factors (Snail).
Main Results:
- JPJD significantly inhibited TGF-β-induced CRC cell invasion and migration in a dose-dependent manner.
- JPJD increased E-cadherin expression and decreased Vimentin expression, suppressing EMT.
- In vivo, JPJD reduced liver and lung metastasis and prolonged survival in tumor-bearing mice, while modulating key protein expressions in tumor tissues.
Conclusions:
- JPJD effectively inhibits TGF-β-induced EMT in colorectal cancer.
- The mechanism involves the modulation of the TGF-β/Smad signaling pathway, impacting Snail and E-cadherin expression.
- JPJD demonstrates significant potential as an alternative therapeutic agent for preventing CRC metastasis.
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