Journal of ethnopharmacology · 2025
Qingre Huayu Jianpi decoction suppresses colorectal tumorigenesis by inhibiting cancer stem cells and cancer-associated fibroblasts.
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Guirong Chen, Lili Huang, Guifang Deng, Weiqi Lu, Xiongbo Guo, Fan Xiao, Zhenyu Niu, Jinbin Song, Gang Chen, Lina Zhao, Wenfeng Guo, Qun Du, Yanwu Li
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Heat-clearing, stasis-dissolving, and spleen-fortifying constitute a fundamental treatment strategy in Traditional Chinese medicine (TCM) for intestinal neoplasm management. Qingre Huayu Jianpi decoction (QHJ) has good prevention and treatment effects on colitis-associated colon cancer (CAC) and sporadic colorectal carcinoma subtypes in clinical application, but its multi-target mechanism of action against intestinal tumors requires elucidation through integrative pharmacology approaches.
AIM OF THE STUDY: To evaluate the preventive and therapeutic effects of Qingre Huayu Jianpi decoction (QHJ) on colon cancer, particularly focusing on its impact on colon cancer stem cell (CSC) proliferation and cancer-associated fibroblast (CAF) activation.
METHODS: An azoxymethane (AOM) and dextran sulfate sodium (DSS)-induced colorectal cancer (CRC) mouse model was used to assess the effects of QHJ on tumor count, pathological morphology, and collagen deposition in the colon. Gut organoids and fibroblasts isolated from CRC patient tissues were cultured to explore the effect of QHJ. Then, a PDOX (patient-derived organoids-based xenograft) experiment was performed to evaluate the inhibitory effect of QHJ on xenograft tumorigenesis in nude mice. Immunohistochemistry, immunofluorescence, and Western blot analyses were employed to detect the expression levels of markers such as Ki67, CD44, FAP, α-SMA, COL1A1, COL3A1, FN, LN, and proteins associated with the Wnt signaling pathway.
RESULTS: We found that QHJ significantly suppressed the number and volume of tumors in CRC mice, lowered pathological scores, and decreased collagen deposition in affected mucosal regions. QHJ treatment inhibited the viability of colon cancer organoids from CRC patients and HCT116 cells in vitro and can inhibit CAF activation and migration. Protein analysis indicated upregulation of RNF43 and downregulation of ZNRF3 and β-Catenin after QHJ treatment, alongside reductions in Ki67, CD44, α-SMA, COL1A1, Collagen Ⅳ, FN, and LN expression levels. QHJ reduces the number of cancer cells in the tumors of nude mice transplanted subcutaneously with human colon cancer organoids and CAFs.
CONCLUSION: This study demonstrates that QHJ inhibits cancer cell proliferation, cancer-associated fibroblast activation, and extracellular matrix collagen deposition in the tumor microenvironment of colon cancer. The comprehensive therapeutic advantages of QHJ in the prevention and treatment of colorectal cancer were revealed.
AIM OF THE STUDY: To evaluate the preventive and therapeutic effects of Qingre Huayu Jianpi decoction (QHJ) on colon cancer, particularly focusing on its impact on colon cancer stem cell (CSC) proliferation and cancer-associated fibroblast (CAF) activation.
METHODS: An azoxymethane (AOM) and dextran sulfate sodium (DSS)-induced colorectal cancer (CRC) mouse model was used to assess the effects of QHJ on tumor count, pathological morphology, and collagen deposition in the colon. Gut organoids and fibroblasts isolated from CRC patient tissues were cultured to explore the effect of QHJ. Then, a PDOX (patient-derived organoids-based xenograft) experiment was performed to evaluate the inhibitory effect of QHJ on xenograft tumorigenesis in nude mice. Immunohistochemistry, immunofluorescence, and Western blot analyses were employed to detect the expression levels of markers such as Ki67, CD44, FAP, α-SMA, COL1A1, COL3A1, FN, LN, and proteins associated with the Wnt signaling pathway.
RESULTS: We found that QHJ significantly suppressed the number and volume of tumors in CRC mice, lowered pathological scores, and decreased collagen deposition in affected mucosal regions. QHJ treatment inhibited the viability of colon cancer organoids from CRC patients and HCT116 cells in vitro and can inhibit CAF activation and migration. Protein analysis indicated upregulation of RNF43 and downregulation of ZNRF3 and β-Catenin after QHJ treatment, alongside reductions in Ki67, CD44, α-SMA, COL1A1, Collagen Ⅳ, FN, and LN expression levels. QHJ reduces the number of cancer cells in the tumors of nude mice transplanted subcutaneously with human colon cancer organoids and CAFs.
CONCLUSION: This study demonstrates that QHJ inhibits cancer cell proliferation, cancer-associated fibroblast activation, and extracellular matrix collagen deposition in the tumor microenvironment of colon cancer. The comprehensive therapeutic advantages of QHJ in the prevention and treatment of colorectal cancer were revealed.