Journal of ethnopharmacology · 2025
Jiedu Sangen Decoction inhibits Epithelial-mesenchymal transition of colon adenocarcinoma via POU4F2/Hedgehog pathway.
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Wang Pei-Pei, Liu Qing-Yang, Liu Hong-Xi, Xia Yu-Wei, Shen De-Yi, Shen Min-He, Ruan Shan-Ming, Sun Lei-Tao
Аннотация
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.
Предметные рубрики MeSH
Epithelial-Mesenchymal TransitionHumansColonic NeoplasmsAnimalsSignal TransductionAdenocarcinomaDrugs, Chinese HerbalMice, Inbred BALB CMice, NudeHedgehog ProteinsCell Line, TumorCell MovementCell ProliferationMiceAntineoplastic Agents, PhytogenicXenograft Model Antitumor AssaysMaleHomeodomain Proteins