Journal of ethnopharmacology · 2026
Huangqi Jianzhong decoction inhibits CRC invasion through the modulation of BCLAF1-mediated glycolysis.
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Liu Xinlu, Cui Yuying, Liu Hua, Zhang Ran, Zhang Yao, Song Huiyi
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Huangqi Jianzhong decoction (HQJZ) is a well-known traditional Chinese medicine used to treat gastrointestinal diseases because of its beneficial effects on Qi and the spleen. Its potential effect on gastric cancer has also been well demonstrated, but its multitarget mechanisms in the treatment of CRC remain unclear, limiting its scientific development.
AIM OF THE STUDY: This study aimed to clarify the role and specific mechanism of HQJZ in combating CRC and identify the key proteins it modulates and the specific mechanism involved.
MATERIALS AND METHODS: We performed cellular function experiments to validate the effects of HQJZ on CRC cell activity, apoptosis, proliferation, migration and invasion. Network pharmacology was combined with differential proteomics to identify key modulated proteins. Western blot, immunofluorescence and lactic acid assays were used to clarify the specific mechanism involved.
RESULTS: The suppressive effects of HQJZ on the proliferation, migration and invasion of CRC cells were verified. By combining network pharmacology and differential proteomics, we identified BCL2-associated transcription factor 1 (BCLAF1) as one of the key proteins involved in the inhibition of the CRC malignant phenotype by HQJZ. Mechanistic studies revealed that HQJZ associating with BCLAF1 to inhibit glycolytic metabolism and lactic acid production in CRC cells and increase programmed cell death ligand 1 (PD-L1) expression on CRC cell membranes.
CONCLUSIONS: We reveal that HQJZ inhibits CRC malignancy. Modulating and inhibiting BCLAF1-mediated glycolysis to increase PD-L1 expression on CRC cell membranes may affect the sensitivity of CRC cells to immunotherapy, but further study is needed. Our study provides new insights into the treatment of CRC by HQJZ.
AIM OF THE STUDY: This study aimed to clarify the role and specific mechanism of HQJZ in combating CRC and identify the key proteins it modulates and the specific mechanism involved.
MATERIALS AND METHODS: We performed cellular function experiments to validate the effects of HQJZ on CRC cell activity, apoptosis, proliferation, migration and invasion. Network pharmacology was combined with differential proteomics to identify key modulated proteins. Western blot, immunofluorescence and lactic acid assays were used to clarify the specific mechanism involved.
RESULTS: The suppressive effects of HQJZ on the proliferation, migration and invasion of CRC cells were verified. By combining network pharmacology and differential proteomics, we identified BCL2-associated transcription factor 1 (BCLAF1) as one of the key proteins involved in the inhibition of the CRC malignant phenotype by HQJZ. Mechanistic studies revealed that HQJZ associating with BCLAF1 to inhibit glycolytic metabolism and lactic acid production in CRC cells and increase programmed cell death ligand 1 (PD-L1) expression on CRC cell membranes.
CONCLUSIONS: We reveal that HQJZ inhibits CRC malignancy. Modulating and inhibiting BCLAF1-mediated glycolysis to increase PD-L1 expression on CRC cell membranes may affect the sensitivity of CRC cells to immunotherapy, but further study is needed. Our study provides new insights into the treatment of CRC by HQJZ.