ArticleAmerican journal of translational research2026
Yishen Quyu Lishi Formula suppresses multiple myeloma growth via ERK/mTOR-mediated inhibition of protective autophagy and induction of apoptosis.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo evaluate the anti-tumor effect of Yishen Quyu Lishi Formula (YSQYLSF) on multiple myeloma (MM) and to determine whether this effect is mediated by extracellular signal-regulated kinase/mammalian target of rapamycin (ERK/mTOR)-regulated protective autophagy and apoptosis.
methodsH929 xenograft-bearing nude mice were treated with YSQYLSF, bortezomib (BO), or their combination for 21 days. Tumor growth, body weight, histopathology, immunohistochemistry, reverse transcription quantitative polymerase chain reaction (RT-qPCR), Western blotting, and ribonucleic acid sequencing (RNA-Seq) were performed. H929 cells were further used for cell viability assays, green fluorescent protein-microtubule-associated protein 1 light chain 3 (GFP-LC3) imaging, flow cytometry, Western blotting, and rapamycin rescue assays.
resultsYSQYLSF reduced xenograft growth and, when combined with BO, produced a potent anti-tumor effect without significant weight loss or obvious liver and kidney damage. RNA-Seq identified 802 differentially expressed genes, with enrichment in mitogen-activated protein kinase (MAPK), mammalian target of rapamycin (mTOR), autophagy, apoptosis, inflammatory, and immune-related pathways. YSQYLSF increased the phosphorylated ERK/ERK and phosphorylated mTOR/mTOR ratios, decreased LC3-II/LC3-I, increased p62 accumulation, and enhanced the Bax/Bcl-2 and cleaved caspase-3/caspase-3 ratios. In vitro, YSQYLSF reduced H929 cell viability, decreased autophagosome formation, and promoted apoptosis. Rapamycin partially restored autophagy and attenuated apoptosis.
conclusionsYSQYLSF inhibits MM growth by activating the ERK/mTOR pathway, suppressing protective autophagy, and promoting mitochondrial apoptosis. Transcriptomic data also suggest additional immune- and inflammation-related mechanisms that require further validation.
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