Jiedu Sangen Decoction inhibits Epithelial-mesenchymal transition of colon adenocarcinoma via POU4F2/Hedgehog pathway.
1/5 보강
[ETHNOPHARMACOLOGICAL RELEVANCE] Jiedu Sangen Decoction (JSD), a traditional Chinese medicine formulation used for colorectal cancer (CRC) in East China, is a multi-component and multi-target agent wh
APA
Wang PP, Liu QY, et al. (2026). Jiedu Sangen Decoction inhibits Epithelial-mesenchymal transition of colon adenocarcinoma via POU4F2/Hedgehog pathway.. Journal of ethnopharmacology, 356, 120752. https://doi.org/10.1016/j.jep.2025.120752
MLA
Wang PP, et al.. "Jiedu Sangen Decoction inhibits Epithelial-mesenchymal transition of colon adenocarcinoma via POU4F2/Hedgehog pathway.." Journal of ethnopharmacology, vol. 356, 2026, pp. 120752.
PMID
41106566 ↗
Abstract 한글 요약
[ETHNOPHARMACOLOGICAL RELEVANCE] Jiedu Sangen Decoction (JSD), a traditional Chinese medicine formulation used for colorectal cancer (CRC) in East China, is a multi-component and multi-target agent whose mechanisms remain unclear.
[AIM OF THE STUDY] This study evaluated the antitumor efficacy of JSD and investigated its mechanism of action via the POU4F2/Hedgehog signaling axis and epithelial-mesenchymal transition (EMT) cascade.
[MATERIALS AND METHODS] UPLC-Q/TOF-MS identified quality control markers in JSD. Anti-metastatic effects were assessed using colony formation, wound healing, and Transwell assays in colon adenocarcinoma (COAD) cells. EMT and Hedgehog (Hh) pathway markers were examined by Western blot and RT-qPCR. An allograft tumor model validated in vivo efficacy, and bioinformatics analysis correlated POU4F2 expression with COAD prognosis.
[RESULTS] JSD inhibited COAD cell proliferation, migration, and invasion. Mechanistically, it suppressed the POU4F2/Hedgehog axis, reversing EMT via E-cadherin upregulation and N-cadherin downregulation. These findings were consistent in vitro, where JSD also attenuated tumor growth.
[CONCLUSION] JSD suppresses COAD metastasis by inhibiting EMT through the POU4F2/Hh pathway, highlighting its potential as an integrative therapy.
[AIM OF THE STUDY] This study evaluated the antitumor efficacy of JSD and investigated its mechanism of action via the POU4F2/Hedgehog signaling axis and epithelial-mesenchymal transition (EMT) cascade.
[MATERIALS AND METHODS] UPLC-Q/TOF-MS identified quality control markers in JSD. Anti-metastatic effects were assessed using colony formation, wound healing, and Transwell assays in colon adenocarcinoma (COAD) cells. EMT and Hedgehog (Hh) pathway markers were examined by Western blot and RT-qPCR. An allograft tumor model validated in vivo efficacy, and bioinformatics analysis correlated POU4F2 expression with COAD prognosis.
[RESULTS] JSD inhibited COAD cell proliferation, migration, and invasion. Mechanistically, it suppressed the POU4F2/Hedgehog axis, reversing EMT via E-cadherin upregulation and N-cadherin downregulation. These findings were consistent in vitro, where JSD also attenuated tumor growth.
[CONCLUSION] JSD suppresses COAD metastasis by inhibiting EMT through the POU4F2/Hh pathway, highlighting its potential as an integrative therapy.
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
- Epithelial-Mesenchymal Transition
- Humans
- Colonic Neoplasms
- Animals
- Signal Transduction
- Adenocarcinoma
- Drugs
- Chinese Herbal
- Mice
- Inbred BALB C
- Nude
- Hedgehog Proteins
- Cell Line
- Tumor
- Cell Movement
- Cell Proliferation
- Antineoplastic Agents
- Phytogenic
- Xenograft Model Antitumor Assays
- Male
- Homeodomain Proteins
- Colon adenocarcinoma
- Epithelial-mesenchymal transition
- Hedgehog pathway
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