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Trdmt1 3'-非翻译区在白血病 HL-60 细胞分化中作为竞争性内源性 RNA 发挥作用。

Trdmt1 3'-untranslated region functions as a competing endogenous RNA in leukemia HL-60 cell differentiation.

机构信息

Institute of Translational Medicine, Navy Medical University, Shanghai, China.

Department of Embryology and Histology, Navy Medical University, Shanghai, China.

出版信息

Braz J Med Biol Res. 2020 Dec 9;54(2):e9869. doi: 10.1590/1414-431X20209869. eCollection 2020.

DOI:10.1590/1414-431X20209869
PMID:33331537
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7727116/
Abstract

Severe blockage in myeloid differentiation is the hallmark of acute myeloid leukemia (AML). Trdmt1 plays an important role in hematopoiesis. However, little is known about the function of Trdmt1 in AML cell differentiation. In the present study, Trdmt1 was up-regulated and miR-181a was down-regulated significantly during human leukemia HL-60 cell differentiation after TAT-CT3 fusion protein treatment. Accordingly, miR-181a overexpression in HL-60 cells inhibited granulocytic maturation. In addition, our "rescue" assay demonstrated that Trdmt1 3'-untranslated region promoted myeloid differentiation of HL-60 cells by sequestering miR-181a and up-regulating C/EBPα (a critical factor for normal myelopoiesis) via its competing endogenous RNA (ceRNA) activity on miR-181a. These findings revealed an unrecognized role of Trdmt1 as a potential ceRNA for therapeutic targets in AML.

摘要

髓系分化严重受阻是急性髓系白血病 (AML) 的特征。Trdmt1 在造血中发挥重要作用。然而，关于 Trdmt1 在 AML 细胞分化中的功能知之甚少。在本研究中，TAT-CT3 融合蛋白处理后，人白血病 HL-60 细胞分化过程中 Trdmt1 上调，miR-181a 明显下调。因此，HL-60 细胞中 miR-181a 的过表达抑制粒细胞成熟。此外，我们的“挽救”实验表明，Trdmt1 3'非翻译区通过其竞争性内源 RNA (ceRNA) 活性结合 miR-181a 并上调 C/EBPα（正常髓系发生的关键因子），从而促进 HL-60 细胞的髓系分化。这些发现揭示了 Trdmt1 作为 AML 治疗靶点的潜在 ceRNA 的作用尚未被认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/e84de6110d63/1414-431X-bjmbr-54-2-e9869-gf006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/fb61552e6180/1414-431X-bjmbr-54-2-e9869-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/005f13ea8fe0/1414-431X-bjmbr-54-2-e9869-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/1cb4ca428930/1414-431X-bjmbr-54-2-e9869-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/1f8222d21e66/1414-431X-bjmbr-54-2-e9869-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/75f03556309b/1414-431X-bjmbr-54-2-e9869-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/e84de6110d63/1414-431X-bjmbr-54-2-e9869-gf006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/fb61552e6180/1414-431X-bjmbr-54-2-e9869-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/005f13ea8fe0/1414-431X-bjmbr-54-2-e9869-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/1cb4ca428930/1414-431X-bjmbr-54-2-e9869-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/1f8222d21e66/1414-431X-bjmbr-54-2-e9869-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/75f03556309b/1414-431X-bjmbr-54-2-e9869-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8931/7727116/e84de6110d63/1414-431X-bjmbr-54-2-e9869-gf006.jpg

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