دورية أكاديمية
Netrin-1 inducing antiapoptotic effect of acute myeloid leukemia cells in a concentration-dependent manner through the Unc-5 netrin receptor B-focal adhesion kinase axis
| العنوان: | Netrin-1 inducing antiapoptotic effect of acute myeloid leukemia cells in a concentration-dependent manner through the Unc-5 netrin receptor B-focal adhesion kinase axis |
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| المؤلفون: | Kainan Zhang, Xizhou An, Yao Zhu, Lan Huang, Xinyuan Yao, Xing Zeng, Shaoyan Liang, Jie Yu |
| المصدر: | Cancer Biology & Therapy, Vol 24, Iss 1 (2023) |
| بيانات النشر: | Taylor & Francis Group, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| مصطلحات موضوعية: | netrin-1, acute myeloid leukemia, unc5b, fak-akt, apoptosis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
| الوصف: | Acute myeloid leukemia (AML) is a hematological malignancy that commonly occurs in children. The prognosis of pediatric AML is relatively poor, thus threatening the patient’s survival. The aberrant expression of the axon guidance factor, netrin-1, is observed in various types of malignancies, and it participates in the proliferation and apoptosis of tumor cells. Herein, we aimed to explore the role of netrin-1 in AML cells. Netrin-1 is highly expressed in AML patients. Proliferation and anti-apoptosis were observed in AML cells treated with netrin-1. The interaction between netrin-1 and Unc-5 netrin receptor B (UNC5B) was detected through coimmunoprecipitation, and UNC5B ribonucleic acid interference restrained the influence of netrin-1 on the AML cells. The phosphorylation of focal adhesion kinase-protein kinase B (FAK-Akt) was upregulated in AML cells treated with netrin-1. Both FAK and Akt inhibitors abrogated the effects of netrin-1 on the proliferation and apoptosis of AML cells. In conclusion, netrin-1 could promote the growth and reduce the apoptosis of AML cells in a concentration-dependent manner, and that these effects were mediated by activating the FAK-Akt signaling pathway via the UNC5B. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1538-4047 1555-8576 15384047 |
| Relation: | https://doaj.org/toc/1538-4047; https://doaj.org/toc/1555-8576 |
| DOI: | 10.1080/15384047.2023.2200705 |
| URL الوصول: | https://doaj.org/article/f38188dc389f47c28c10c5c78cf3efbb |
| رقم الأكسشن: | edsdoj.f38188dc389f47c28c10c5c78cf3efbb |
| قاعدة البيانات: | Directory of Open Access Journals |
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Full Text Finder | تدمد: | 15384047 15558576 |
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| DOI: | 10.1080/15384047.2023.2200705 |