ASAH1 通过 DUSP5 抑制驱动的 MAP 激酶途径激活促进 TNBC , 并代表治疗脆弱性。
Mesh : Humans Triple Negative Breast Neoplasms / pathology genetics metabolism drug therapy Acid Ceramidase / metabolism genetics Dual-Specificity Phosphatases / metabolism genetics Female Cell Line, Tumor MAP Kinase Signaling System / drug effects Cell Proliferation / drug effects Animals Gene Expression Regulation, Neoplastic / drug effects Mice, Nude Mice Proto-Oncogene Proteins c-akt / metabolism Tumor Suppressor Protein p53 / metabolism genetics Phosphatidylinositol 3-Kinases / metabolism Signal Transduction / drug effects
来 源:
DOI:10.1038/s41419-024-06831-2
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