SMYD2 (SET And MYND Domain Containing 2)

Moreover, we will also briefly discuss the contradiction points in existing studies, provide novel ideas about further study on SMYD2 structure and inhibitor development and finally, discuss the new aspects in further studies of SMYD2. Hopefully, this review stimulates new ideas in drug development for the treatment of cancer and aging-related diseases, maximizes human life, and benefit society.

The identification of TRAPM and the RC3 subtype enhances our understanding of BC heterogeneity and highlights potential therapeutic targets. This study provides a foundation for personalized treatment strategies by clarifying the biological significance and clinical relevance of the RC3 subtype.

SMYD2 functions as an oncogene in melanoma by epigenetically upregulating antioxidant genes SOD1 and GPX1, thereby alleviating oxidative stress and driving lipid reprogramming. These findings uncover a novel SMYD2-oxidative stress-lipid metabolism axis and highlight SMYD2 as a potential therapeutic target in melanoma.

Conclusions. This study's findings validate OC as a novel lead entity for NEPC management by targeting the ROR2-ASCL1-SMYD2-EZH2-c-MET axis.

Collectively, these results indicated that Casticin suppresses and sensitizes non-small-cell lung cancer cells to EGFR-TKIs. Casticin may serve as a sensitizing agent by targeting SMYD2 to improve the efficacy of EGFR-TKIs.

This study elucidates specific features associated with the p53 regulatory pathway, particularly SMYD2, and its relationship with the onset and progression of CESC. Furthermore, SMYD2 may serve as a prognostic biomarker for individuals diagnosed with CESC, offering new insights for the development of clinical treatment strategies.

BBH may inhibit HCC tumorigenesis by disrupting amino acid metabolism and holds potential as a therapeutic agent for HCC.

A metastasis-clonogenicity animal study model using female nude mice subjected to tail vein injection of MDA-MB-231-Luc TNBC cells also revealed the effective synergy of the combined OC-LA, 5 mg/kg each, compared to their individual therapies and VC. Thus, EVOO cultivars rich in OC with optimal LA content can be useful nutraceuticals for invasive hormone-dependent BC and TNBC progression and metastasis.

Additionally, SMYD2 and SMYD3 are involved in the pathogenesis of acute kidney injury. This review summarizes the roles of these two lysine methyltransferases in renal diseases, highlights their mechanisms, and emphasizes their potential as therapeutic targets for kidney disorders.

Functional assays demonstrated that SMYD2 promoted GC cell proliferation, invasion, and migration in vitro. These findings established SMYD2 is a major oncogene that can serve as a candidate diagnostic and prognostic biomarker for GC.

Our study reveals that SMYD2 is an important epigenetic mediator that activates BMP4/R-SMADs/ID3 axis, leading to enhanced stemness and sorafenib resistance. Thus, SMYD2 might represent a potential biomarker and future epigenetic therapeutic target for sorafenib resistance of HCC.

Our study established a robust metabolism-based prognostic model for SCLC that effectively stratifies patients into risk groups with distinct survival outcomes, immune profiles, and drug sensitivity patterns. Functional validation experiments confirmed MOCS2 as an important regulator of SCLC cell proliferation and migration, providing valuable insights for treatment selection and prognosis prediction in SCLC.