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KIF22 promotes multiple myeloma progression by regulating the CDC25C/CDK1/cyclinB1 pathway.
Meng Zhai1,2, Jiyu Miao1,2, Ru Zhang1,2
1Department of Hematology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Journal of Cancer Research and Clinical Oncology
|May 7, 2024
Summary
Kinesin family member 22 (KIF22) promotes multiple myeloma (MM) progression by regulating cell proliferation and the cell cycle. Targeting KIF22 and its downstream CDC25C pathway offers a potential therapeutic strategy for MM patients.
Area of Science:
- Hematological Malignancies
- Molecular Biology
- Cancer Research
Background:
- Multiple myeloma (MM) is an incurable hematological malignancy with unknown pathogenesis.
- Malignant plasma B cells proliferate clonally within the bone marrow in MM.
Purpose of the Study:
- To investigate the role of kinesin family member 22 (KIF22) in the pathogenesis of multiple myeloma (MM).
- To elucidate the molecular mechanisms underlying KIF22's function in MM.
Main Methods:
- KIF22 expression analysis in MM patients using public datasets and clinical samples.
- In vitro assays in MM cell lines and in vivo subcutaneous xenograft models in nude mice.
- Chromatin immunoprecipitation (ChIP) and luciferase reporter assays to determine regulatory mechanisms.
Main Results:
- KIF22 expression in MM patients correlates with clinical features (gender, LDH, β2-MG, tumor cell percentage) and predicts poor prognosis.
- Altered KIF22 expression impacts MM cell proliferation in vitro and tumor growth in vivo, causing G2/M cell cycle arrest.
- KIF22 directly regulates CDC25C transcription and indirectly affects its expression via the ERK pathway, influencing the CDC25C/CDK1/cyclinB1 pathway.
Conclusions:
- KIF22 promotes MM cell proliferation and cell cycle progression by regulating CDC25C and its downstream pathway.
- KIF22's role in MM pathogenesis suggests it as a potential therapeutic target for multiple myeloma.
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