Cytoplasmic LMO2-LDB1 Complex Activates STAT3 Signaling through Interaction with gp130-JAK in Glioma Stem Cellsopen access
- Authors
- Park, Cheol Gyu; Choi, Sang-Hun; Lee, Seon Yong; Eun, Kiyoung; Park, Min Gi; Jang, Junseok; Jeong, Hyeon Ju; Kim, Seong Jin; Jeong, Sohee; Lee, Kanghun; Kim, Hyunggee
- Issue Date
- 7월-2022
- Publisher
- MDPI
- Keywords
- cancer stem cells; glioblastoma; glioma stem cells; LMO2; STAT3
- Citation
- CELLS, v.11, no.13
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELLS
- Volume
- 11
- Number
- 13
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/142766
- DOI
- 10.3390/cells11132031
- ISSN
- 2073-4409
- Abstract
- The oncogenic role of nuclear LIM domain only 2 (LMO2) as a transcriptional regulator is well established, but its function in the cytoplasm is largely unknown. Here, we identified LMO2 as a cytoplasmic activator for signal transducer and activator of transcription 3 (STAT3) signaling in glioma stem cells (GSCs) through biochemical and bioinformatics analyses. LMO2 increases STAT3 phosphorylation by interacting with glycoprotein 130 (gp130) and Janus kinases (JAKs). LMO2-driven activation of STAT3 signaling requires the LDB1 protein and leads to increased expression of an inhibitor of differentiation 1 (ID1), a master regulator of cancer stemness. Our findings indicate that the cytoplasmic LMO2-LDB1 complex plays a crucial role in the activation of the GSC signaling cascade via interaction with gp130 and JAK1/2. Thus, LMO2-LDB1 is a bona fide oncogenic protein complex that activates either the JAK-STAT signaling cascade in the cytoplasm or direct transcriptional regulation in the nucleus.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
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