ArticleBreast cancer (Tokyo, Japan)2022
Overexpression of MCAM induced by SMYD2-H3K36me2 in breast cancer stem cell properties.
Article in Breast cancer (Tokyo, Japan), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- BCL11B predetermines a persister state in breast cancer that is reversed by TNFα.Science advances · 2026Article
- SMYD family in cancer: epigenetic regulation and molecular mechanisms of cancer proliferation, metastasis, and drug resistance.Experimental & molecular medicine · 2024Review
- CD146, a therapeutic target involved in cell plasticity.Science China. Life sciences · 2024Review
- Lysine Methyltransferases SMYD2 and SMYD3: Emerging Targets in Kidney Diseases.Kidney diseases (Basel, Switzerland)Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMelanoma cell adhesion molecule (MCAM) is highly expressed in various malignancies. However, studies on the effects of MCAM on stemness of cancer stem cells are limited. Here, we aimed to explore the relationship between MCAM and stem cell phenotype in breast cancer (BC).
methodsWe analyzed the genes differentially expressed in BC from the oncomine database, followed by TCGA-BRCA database validation. We then used gene set enrichment analysis to analyze the signaling pathways enriched to the relevant genes, followed by loss-of-function experiments to analyze the role of MCAM in the growth of BC cells and the maintenance of stem cell properties. We analyzed the cause for the MCAM overexpression using ChIP-seq and clarified the upstream mechanism by constructing SE-Deleted cells. Finally, the role of SMYD2 in the growth of BC cells and the maintenance of stem cell properties were verified by rescue experiments.
resultsMCAM was significantly overexpressed in BC, which predicted somber prognosis in patients. Knockdown of MCAM drastically hindered the growth and metastasis of BC cells in vitro and in vivo. Subsequently, the MCAM promoter was observed to have significant H3K36me2 modification and that SMYD2 could significantly promote the expression of MCAM. In addition, further overexpression of SMYD2 in cells with MCAM knockdown increased MCAM expression and promoted the growth as well as stemness of BC cells.
conclusionSMYD2 can elevate the expression of MCAM by promoting its H3K36me2 modification, which in turn expedites the growth and stem cell properties of BC cells.
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