Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin

Abstract

The objective was to explore the pharmacological mechanism of modified shengmaiyin (MSMY) in the treatment of acute lymphoblastic leukemia (ALL) by network pharmacology analysis. The effective components and predicted targets of MSMY were collected from TCMSP and Swiss target prediction databases, and the related targets of ALL were screened by GeneCards and DisGeNET. The core targets and related signaling pathways of MSMY active ingredients for the treatment of ALL were predicted by protein-protein interaction network (PPI), gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. We identified 172 potential targets for the active components of MSMY, 538 disease targets associated with ALL, and 59 common gene targets. PPI network showed that 27 targets such as triptolide, RAC-alpha serine/threonine-protein kinase (AKT1), vascular endothelial growth factor A and Caspase-3 (CASP3) were the core targets. KEGG enrichment analysis related signaling pathways included cancer pathway, phosphatidylinositol 3 kinase, PI-3K/protein kinase B (PI3K-Akt) signaling pathway, apoptosis and mitogen-activated protein kinase (MAPK) signaling pathway and IL-17 signaling pathway. The effective active components and potential therapeutic targets of MSMY in the treatment of ALL were initially identified by comprehensive network pharmacology, which provides a theoretical basis for further study of the material basis and molecular mechanism of MSMY in the treatment of ALL.

TCM targets ferroptosis: potential treatments for cancer

“…(Zheng et al, 2009;Liu et al, 2016;Wang et al, 2020b;Xu et al, 2021b). Sheng Mai Yin has previously been reported to have therapeutic effects on acute lymphoblastic leukemia (Guo et al, 2023), cardiac hypertrophy (Ming et al, 2022), heart failure (Kan et al, 2022), type 2 diabetes mellitus (T2DM) (Li et al, 2019). In addition, Sheng Mai Yin has been shown to inhibit the toxic side effects of doxorubicin and induced ferroptosis by modulating HMOX1, assisting cancer treatment and reducing patient complications (Meng et al, 2023).…”