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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Li, Yan Zhang, Zimu Yu, Juanjuan Yin, Hongli Chu, Xinran Cao, Haibo Tao, Yanfang Zhang, Yongping Li, Zhiheng Wu, Shuiyan Hu, Yizhou Zhu, Frank Gao, Jizhao Wang, Xiaodong Zhou, Bi Jiao, Wanyan Wu, Yumeng Yang, Yang Chen, Yanling Zhuo, Ran Yang, Ying Zhang, Fenli Shi, Lei Hu, Yixin Pan, Jian Hu, Shaoyan |
| Abstract | Background Despite significant progress in the prognosis of pediatric T-cell acute lymphoblastic leukemia (T-ALL) in recent decades, a notable portion of children still confronts challenges such as treatment resistance and recurrence, leading to limited options and a poor prognosis. LIM domain-binding protein 1 (LDB1) has been confirmed to exert a crucial role in various physiological and pathological processes. In our research, we aim to elucidate the underlying function and mechanisms of LDB1 within the background of T-ALL. Methods Employing short hairpin RNA (shRNA) techniques, we delineated the functional impact of LDB1 in T-ALL cell lines. Through the application of RNA-Seq, CUT&Tag, and immunoprecipitation assays, we scrutinized master transcription factors cooperating with LDB1 and identified downstream targets under LDB1 regulation. Results LDB1 emerges as a critical transcription factor co-activator in cell lines derived from T-ALL. It primarily collaborates with master transcription factors (ERG, ETV6, IRF1) to cooperatively regulate the transcription of downstream target genes. Both in vitro and in vivo experiments affirm the essential fuction of LDB1 in the proliferation and survival of cell lines derived from T-ALL, with MYB identified as a significant downstream target of LDB1. Conclusions To sum up, our research establishes the pivotal fuction of LDB1 in the tumorigenesis and progression of T-ALL cell lines. Mechanistic insights reveal that LDB1 cooperates with ERG, ETV6, and IRF1 to modulate the expression of downstream effector genes. Furthermore, LDB1 controls MYB through remote enhancer modulation, providing valuable mechanistic insights into its involvement in the progression of T-ALL. |
| Related Links | https://jeccr.biomedcentral.com/counter/pdf/10.1186/s13046-024-03199-1.pdf |
| Ending Page | 20 |
| Page Count | 20 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 17569966 |
| DOI | 10.1186/s13046-024-03199-1 |
| Journal | Journal of Experimental & Clinical Cancer Research |
| Issue Number | 1 |
| Volume Number | 43 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2024-10-09 |
| Access Restriction | Open |
| Subject Keyword | Cancer Research Immunology Apoptosis Oncology T-cell acute lymphoblastic leukemia,LDB1 CUT&Tag analysis MYB MBZ |
| Content Type | Text |
| Resource Type | Article |
| Subject | Oncology Cancer Research |
| Journal Impact Factor | 11.4/2023 |
| 5-Year Journal Impact Factor | 11.4/2023 |
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