Observational studyOncology reports2021
JMJD2C triggers the growth of multiple myeloma cells via activation of β‑catenin.
Observational study in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Dujieqing decoction suppresses multiple myeloma growth by inhibiting the Wnt/β-catenin pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Multiple myeloma: signaling pathways and targeted therapy.Molecular biomedicine · 2024Review
- Identification ofOpen life sciences · 2024Article
- The promotive role of lncRNA MIR205HG in proliferation, invasion, and migration of melanoma cells via the JMJD2C/ALKBH5 axis.PloS one · 2024Article
- Network pharmacology- and molecular docking-based investigation of the therapeutic potential and mechanism of daucosterol against multiple myeloma.Translational cancer research · 2023Article
- Review
- Transcriptomic and Drug Discovery Analyses Reveal Natural Compounds Targeting the KDM4 Subfamily as Promising Adjuvant Treatments in Cancer.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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