ArticleExperimental and therapeutic medicine2023
SETDB1 induces lenalidomide resistance in multiple myeloma cells via epithelial‑mesenchymal transition and PI3K/AKT pathway activation.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- SETDB1 promotes gastric cancer progression via UPR and mTOR pathway.Cancer cell international · 2026Article
- The Role of Histone Methyltransferase SETDB1 in Normal and Malignant Hematopoiesis.Cancer science · 2025Review
- SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.Oncotarget · 2025Review
- Emerging roles of non-coding RNAs in modulating the PI3K/Akt pathway in cancer.Non-coding RNA research · 2025Review
- The SAGA acetyltransferase module is required for the maintenance of MAF and MYC oncogenic gene expression programs in multiple myeloma.Genes & development · 2024Article
- The SAGA acetyltransferase module is required for the maintenance of MAF and MYC oncogenic gene expression programs in multiple myeloma.bioRxiv : the preprint server for biology · 2024Article
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8 authors at 1 institution in 1 country.
Funding
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Abstract
SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) is a histone H3K9 methyltransferase that stimulates cell proliferation by methylating AKT, which contributes to drug resistance in multiple myeloma (MM). Lenalidomide is an immunomodulatory agent widely used in the treatment of MM. However, lenalidomide resistance occurs in patients with MM. Currently, the role of SETDB1 in lenalidomide resistance in MM remains unclear. Thus, the present study aimed to explore the functional association between SETDB1 and lenalidomide resistance in MM. The analysis of GEO datasets revealed that SETDB1 was upregulated in lenalidomide-resistant MM cells and that its expression was associated with poor prognosis of patients with MM. Apoptosis analysis revealed that overexpression of SETDB1 in MM cells significantly decreased apoptosis, while knockdown of SETDB1 increased apoptosis. Furthermore, the IC
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