دورية أكاديمية
Cytoplasmic NEAT1 Suppresses AML Stem Cell Self‐Renewal and Leukemogenesis through Inactivation of Wnt Signaling
العنوان: | Cytoplasmic NEAT1 Suppresses AML Stem Cell Self‐Renewal and Leukemogenesis through Inactivation of Wnt Signaling |
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المؤلفون: | Huiwen Yan, Zhi Wang, Yao Sun, Liangding Hu, Pengcheng Bu |
المصدر: | Advanced Science, Vol 8, Iss 22, Pp n/a-n/a (2021) |
بيانات النشر: | Wiley, 2021. |
سنة النشر: | 2021 |
المجموعة: | LCC:Science |
مصطلحات موضوعية: | acute myeloid leukemia, nuclear paraspeckle assembly transcript 1, translocation, ubiquitination, Wnt, Science |
الوصف: | Abstract As an essential component of paraspeckles, nuclear paraspeckle assembly transcript 1 (NEAT1) localizes in the nucleus, promoting progression of various malignant solid tumors. Herein, an adverse effect of NEAT1 is reported, showing that the short isoform, NEAT1_1 suppresses acute myeloid leukemia (AML) development. NEAT1_1 is downregulated in leukemia stem cells (LSCs) and its decreased expression correlates with recurrence in AML patients. It is demonstrated that NEAT1_1 suppresses leukemogenesis and LSC function but is dispensable for normal hematopoiesis. Mechanistically, NEAT1_1 is released from the nucleus into the cytoplasm of AML cells, regulated by transcription factor C/EBPβ and nuclear protein NAP1L1. Cytoplasmic NEAT1_1 interacts with Wnt component DVL2 and E3 ubiquitin ligase Trim56, facilitates Trim56‐mediated DVL2 degradation, and thus suppresses Wnt signaling. Collectively, the findings show NEAT1_1 is translocated from the nucleus to the cytoplasm and acts as a tumor suppressor in AML. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2198-3844 71855084 |
العلاقة: | https://doaj.org/toc/2198-3844Test |
DOI: | 10.1002/advs.202100914 |
الوصول الحر: | https://doaj.org/article/b7f2a718550840a79ed60fdfbd44a07eTest |
رقم الانضمام: | edsdoj.b7f2a718550840a79ed60fdfbd44a07e |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 21983844 71855084 |
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DOI: | 10.1002/advs.202100914 |