SSBP1 is a novel prognostic marker and promotes disease progression via p38MAPK signaling pathway in multiple myeloma

Multiple myeloma (MM) remains an incurable disease. Identification of meaningful co‐expressed gene clusters or representative biomarkers of MM may help to identify new pathological mechanisms and promote the development of new therapies. Here, we performed weighted sgene co‐expression network analys...

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Bibliographic Details
Published in:Molecular carcinogenesis 2024-04, Vol.63 (4), p.728-741
Main Authors: Xiao, Pingping, Wang, Jizhen, Li, Tingting, Yang, Apeng, Qiu, Dongbiao, Chen, Junmin, Zeng, Zhiyong
Format: Article
Language:English
Subjects:
Apoptosis
Bioinformatics
Biomarkers
Cell cycle
Cell proliferation
CRISPR
G1 phase
Gene clusters
Multiple myeloma
p38MAPK
Pathology
prognostic marker
Reactive oxygen species
Signal transduction
SSBP1
weighted gene co‐expression network analysis
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Summary:Multiple myeloma (MM) remains an incurable disease. Identification of meaningful co‐expressed gene clusters or representative biomarkers of MM may help to identify new pathological mechanisms and promote the development of new therapies. Here, we performed weighted sgene co‐expression network analysis and a series of bioinformatics analysis to identify single stranded DNA binding protein 1 (SSBP1) as novel hub gene associated with MM development and prognosis. In vitro, CRISPR/cas9 mediated knockdown of SSBP1 can significantly inhibit the proliferation of MM cells through inducing apoptosis and cell cycle arrest in G0/G1 phase. We also found that decreased SSBP1 expression significantly increased mitochondrial reactive oxygen species (mtROS) generation and the level of phosphorylated p38MAPK. Furthermore, it was further verified that disruption of SSBP1 expression could inhibit the tumor growth via p38MAPK pathway in a human myeloma xenograft model. In summary, our study is the first to demonstrate that SSBP1 promotes MM development by regulating the p38MAPK pathway.
ISSN:0899-1987
1098-2744
DOI:10.1002/mc.23684