Chronic restraint stress promotes the mobilization and recruitment of myeloid‐derived suppressor cells through β‐adrenergic‐activated CXCL5‐CXCR2‐Erk signaling cascades
| العنوان: | Chronic restraint stress promotes the mobilization and recruitment of myeloid‐derived suppressor cells through β‐adrenergic‐activated |
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| المؤلفون: | Nasi Liu, Guiping Wang, Youming Wu, Tongtong Xue, Gaoxiang Li, Qian Li, Yuzhu Chen, Yanyong Liu, Dexin Kong, Wei Huang, Nan Yang, Mingyue Cao |
| المصدر: | International Journal of Cancer. 149:460-472 |
| بيانات النشر: | Wiley, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Male, MAPK/ERK pathway, Chemokine CXCL5, Cancer Research, Chemokine, Carcinoma, Hepatocellular, MAP Kinase Signaling System, Adrenergic beta-Antagonists, Receptors, Interleukin-8B, Mice, 03 medical and health sciences, Chemokine receptor, 0302 clinical medicine, Cell Line, Tumor, Animals, CXC chemokine receptors, biology, Chemistry, Myeloid-Derived Suppressor Cells, Liver Neoplasms, Propranolol, Gene Expression Regulation, Neoplastic, Oncology, Tumor progression, CXCL5, 030220 oncology & carcinogenesis, Cancer research, biology.protein, Myeloid-derived Suppressor Cell, Signal transduction, Neoplasm Transplantation, Spleen, Stress, Psychological |
| الوصف: | Myeloid-derived suppressor cells (MDSCs) play an important role in tumor immune escape. Recent studies have shown that MDSCs contribute to tumor progression under psychological stress, but the underlying mechanism of MDSCs mobilization and recruitment remains largely unknown. In the present study, a chronic restraint stress paradigm was applied to the H22 hepatocellular carcinoma (HCC) bearing mice to mimic the psychological stress. We observed that chronic restraint stress significantly promoted HCC growth, as well as the mobilization of MDSCs to spleen and tumor sites from bone marrow. Meanwhile, chronic restraint stress enhanced the expression of C-X-C motif chemokine receptor 2 (CXCR2) and pErk1/2 in bone marrow MDSCs, together with elevated chemokine (C-X-C motif) ligand 5 (CXCL5) expression in tumor tissues. In vitro, the treatments of MDSCs with epinephrine (EPI) and norepinephrine (NE) but not corticosterone (CORT)-treated H22 conditioned medium obviously inhibited T-cell proliferation, as well as enhanced CXCR2 expression and extracellular signal-regulated kinase (Erk) phosphorylation. In vivo, β-adrenergic blockade with propranolol almost completely reversed the accelerated tumor growth induced by chronic restraint stress and inactivated CXCL5-CXCR2-Erk signaling pathway. Our findings support the crucial role of β-adrenergic signaling cascade in the mobilization and recruitment of MDSCs under chronic restraint stress. |
| تدمد: | 1097-0215 0020-7136 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::996e9fab4ec82ec912e47c13e0326ef2Test https://doi.org/10.1002/ijc.33552Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....996e9fab4ec82ec912e47c13e0326ef2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10970215 00207136 |
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