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The non-cell-autonomous function of ID1 promotes AML progression via ANGPTL7 from the microenvironment.

Author: ChangBin-He, ChangChun-Kang, ChenBing-Yi, ChenShu-Bei, ChenXin-Chi, DengChu-Han, DongFangyi, FeiMing-Yue, GaoFei-Fei, HongMing-Hua, HouDan, HuCheng-Long, HuangDan, JiangYi-Lun, JinJia-Cheng, LiXi-Ya, LiZi-Juan, LiuHui, LiuNa, LiuPing, RenYi-Yi, ShenShuhong, SunXiao-Jian, WangLan, WangRou-Jia, WangYong, WuJi-Chuan, WuLing-Yun, XuChun-Hui, XueKai, YanJinsong, YuPeng-Cheng, ZhangJia-Ying, ZhangQun-Ling, ZhaoChong, ZongLi-Juan

Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.
Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.

Overview

This study investigated the role of inhibitor of DNA binding 1 (ID1) in the bone marrow microenvironment (BMM) of acute myeloid leukemia (AML) patients. The study found that ID1 is highly expressed in the AML BMM, particularly in mesenchymal stem cells, and that its expression is induced by BMP6 secreted from AML cells. Knocking out ID1 in mesenchymal cells significantly suppressed AML cell proliferation. The study further revealed that ID1 interacts with RNF4, an E3 ubiquitin ligase, leading to reduced SP1 ubiquitination and increased SP1 protein levels. The study suggests that targeting ID1 in the AML BMM could be a promising therapeutic strategy for AML.
Paper Details　
Original Abstract of the Article :
The bone marrow microenvironment (BMM) can regulate leukemia stem cells (LSCs) via secreted factors. Increasing evidence suggests that dissecting the mechanisms by which the BMM maintains LSCs may lead to the development of effective therapies for the eradication of leukemia. Inhibitor of DNA bindin...See full text at original site
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引用元：
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644073/

データ提供：米国国立医学図書館（NLM）

ID1's Role in Acute Myeloid Leukemia Progression

This study delves into the intricate world of acute myeloid leukemia (AML) progression, exploring the non-cell-autonomous function of ID1, a key transcriptional regulator, in the bone marrow microenvironment (BMM). The research investigates how ID1, highly expressed in the BMM of AML patients, particularly in mesenchymal stem cells, contributes to AML progression. The study's findings reveal that ID1, induced by BMP6 secreted from AML cells, plays a crucial role in promoting AML progression by regulating the production of ANGPTL7 from the BMM, a factor that supports AML cell growth and survival.

ID1: A Key Player in AML Progression

The study's findings highlight the critical role of ID1 in the bone marrow microenvironment (BMM) of AML patients, demonstrating its ability to influence AML progression by regulating the production of ANGPTL7 from mesenchymal stem cells. This research suggests that targeting ID1 and its downstream pathways may offer a promising therapeutic strategy for AML, potentially disrupting the communication between AML cells and the BMM and hindering AML progression.

Navigating the Desert of Leukemia Research

Leukemia is a complex and often aggressive cancer, requiring a multi-faceted approach to treatment. This study sheds light on the crucial role of the bone marrow microenvironment (BMM) in AML progression, highlighting the potential for targeting BMM-specific pathways for therapeutic intervention. The research underscores the importance of understanding the intricate interactions between cancer cells and their surrounding environment, providing valuable insights into the development of novel therapies for AML.

Dr.Camel's Conclusion

This study reveals the critical role of ID1 in the bone marrow microenvironment of acute myeloid leukemia patients, demonstrating its ability to influence AML progression by regulating the production of ANGPTL7. The research underscores the importance of understanding the intricate interactions between cancer cells and their surrounding environment, providing valuable insights into the development of novel therapies for this challenging disease. As we journey through the vast desert of leukemia research, this study serves as a vital oasis, offering hope for new treatment strategies and improved outcomes for patients.
Date :
  1. Date Completed 2023-09-08
  2. Date Revised 2023-11-16
Further Info :

Pubmed ID

37319434

DOI: Digital Object Identifier

PMC10644073

Related Literature

Article Analysis
・Causes of acute myeloid leukemia (aml)
SNS
PICO Info
in preparation
Languages

English

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