pRb / RBL2 - E2F1 / 4 - GCN5 轴通过旁分泌机制调节癌干细胞形成和 G0 期进入 / 退出。
Mesh : Humans Neoplastic Stem Cells / metabolism pathology Paracrine Communication E2F1 Transcription Factor / metabolism genetics Cell Line, Tumor Pancreatic Neoplasms / metabolism pathology genetics E2F4 Transcription Factor / metabolism genetics Animals Carcinoma, Pancreatic Ductal / pathology genetics metabolism Wnt Proteins / metabolism genetics Retinoblastoma Protein / metabolism genetics Breast Neoplasms / metabolism genetics pathology p300-CBP Transcription Factors / metabolism genetics Gene Expression Regulation, Neoplastic Proto-Oncogene Proteins p21(ras) / genetics metabolism Female Cell Proliferation Mice Signal Transduction Drug Resistance, Neoplasm / genetics
来 源:
DOI:10.1038/s41467-024-47680-z
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