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An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
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MYSM1/miR-150/FLT3 inhibits B1a cell proliferation
Xiao-Xia Jiang1, Yu Liu1,2, Hong Li1
1Beijing Institute of Basic Medical Sciences, Beijing, China.
Oncotarget
|September 4, 2016
Summary
Myb Like, SWIRM And MPN Domains 1 (MYSM1) normally limits B1a cell proliferation. MYSM1 deficiency increases B1a cell numbers, suggesting a role in autoimmune diseases like Systemic Lupus Erythematosus (SLE).
Area of Science:
- Immunology
- Molecular Biology
- Epigenetics
Background:
- Aberrant B1a cell expansion is implicated in murine autoimmune diseases.
- The precise mechanisms regulating B1a cell proliferation remain incompletely understood.
Purpose of the Study:
- To investigate the role of Myb Like, SWIRM And MPN Domains 1 (MYSM1) in B1a cell proliferation.
- To elucidate the molecular pathway involving MYSM1 in B1a cell regulation.
Main Methods:
- Murine models of autoimmune disease.
- Analysis of MYSM1's role in B1a cell proliferation.
- Investigating the MYSM1/c-Myc/miR-150/FLT3 signaling axis.
- Flow cytometry analysis of B1 cells in Systemic Lupus Erythematosus (SLE) patients.
Main Results:
- MYSM1 deficiency leads to increased B1a cell proliferation in mice.
- MYSM1 recruits c-Myc to stimulate miR-150 transcription.
- miR-150 negatively regulates FMS-like tyrosine kinase 3 (FLT3) expression in B1a cells.
- Elevated FLT3+ B1 cell percentages observed in SLE patients compared to healthy controls.
Conclusions:
- A novel pathway MYSM1/miR-150/FLT3 inhibits B1a cell proliferation.
- This pathway may play a significant role in the pathogenesis of Systemic Lupus Erythematosus (SLE).
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