Inactivated cGAS‐STING Signaling Facilitates Endocrine Resistance by Forming a Positive Feedback Loop with AKT Kinase in ER+HER2– Breast Cancer - Zhang, Kai‐Ming; Zhao, De‐Chang; Li, Ze‐Yu; Wang, Yan; Liu, Jian‐Nan; Du, Tian; Zhou, Ling; Chen, Yu‐Hong; Yu, Qi‐Chao; Chen, Qing‐Shan; Cai, Rui‐Zhao; Zhao, Zi‐Xuan; et al. (Advanced science, 2024)
Keywords: AKT kinase; Animals; Breast cancer; Breast Neoplasms - drug therapy; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Cancer therapies; Cell Line, Tumor; cGAS‐STING pathway; Disease Models, Animal; Drug Resistance, Neoplasm - genetics; Endocrine therapy; endocrine‐resistant breast cancer; Estrogens; Feedback; Feedback, Physiological; Female; Humans; Immunity (Disease); Interferon; Kinases; Lymphocytes; Medical prognosis; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Nucleotidyltransferases - genetics; Nucleotidyltransferases - metabolism; Phosphorylation; positive feedback loop; Proto-Oncogene Proteins c-akt - genetics; Proto-Oncogene Proteins c-akt - metabolism; Receptor, ErbB-2 - genetics; Receptor, ErbB-2 - metabolism; Receptors, Estrogen - genetics; Receptors, Estrogen - metabolism; Signal Transduction - drug effects; Survival analysis; Tumors; cGAS‐STING pathway; positive feedback loop; endocrine‐resistant breast cancer; AKT kinase