JMJD2C triggers the growth of multiple myeloma cells via activation of β-catenin
Autor: | Ming Lv, Qicai Liu |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Adult
Male Cancer Research Jumonji Domain-Containing Histone Demethylases Cell Kaplan-Meier Estimate Epigenesis Genetic Cell Line Tumor medicine Biomarkers Tumor Humans Viability assay Phosphorylation Promoter Regions Genetic Wnt Signaling Pathway cell viability beta Catenin Aged Cell Proliferation Glycogen Synthase Kinase 3 beta Oncogene Chemistry General Medicine Articles Cell cycle β-catenin Middle Aged Healthy Volunteers Cell biology multiple myeloma DNA Demethylation Gene Expression Regulation Neoplastic Histone Code medicine.anatomical_structure Oncology Apoptosis Catenin Case-Control Studies Jumonji C domain-containing 2 Female Signal transduction |
Zdroj: | Oncology Reports |
ISSN: | 1791-2431 1021-335X |
Popis: | Emerging evidence has indicated that histone modification and its related regulators are involved in the progression of multiple myeloma (MM) cells. In the present study, the expression of Jumonji C domain‑containing 2 (JMJD2) was examined in both MM tissues and healthy controls. The roles of JMJD2C in the progression of MM were further investigated. The results revealed that the expression of JMJD2C, but not that of JMJD2A or JMJD2B, was increased in MM tissues compared with the healthy controls. The overexpression of JMJD2C significantly increased the in vitro growth of MM cells. The inhibitor of the β‑catenin signaling pathway significantly attenuated the JMJD2C‑induced growth of MM cells. Mechanistical analyses indicated that JMJD2C increased the transcription of β‑catenin in MM cells, which may be due to the fact that JMJD2C can directly bind with the promoter of β‑catenin. Furthermore, JMJD2C activated β‑catenin in MM cells via a GSK3β‑dependent manner, which was evidenced by the results demonstrating that the overexpression of GSK3β attenuated the JMJD2C‑induced decrease in the phosphorylation of β‑catenin. On the whole, the findings of the present study demonstrated that JMJD2C promotes the malignancy of MM via the activation of the β‑catenin pathway. These results suggested that JMJD2C may be a potential target for MM treatment. |
Databáze: | OpenAIRE |
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