ArticleCancer science2023
Identification of a novel target of SETD1A histone methyltransferase and the clinical significance in pancreatic cancer.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting RuvBL1 disrupts mitochondrial metabolism and structure in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2026Article
- Canonical and Non-Canonical Functions of Histone H3K4 Methylation Modifiers in Cancer.Cancer science · 2025Review
- Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.Breast cancer research : BCR · 2025Article
- Potential mechanism of circKIAA1429 accelerating the progression of hepatocellular carcinoma.Infectious agents and cancer · 2025Article
- Insights into the mechanisms driven by H3K4 KMTs in pancreatic cancer.The Biochemical journal · 2024Review
- The role of histone post-translational modifications in cancer and cancer immunity: functions, mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- SETD1A-mediated Methylation of H3K4me3 Inhibits Ferroptosis in Non-small Cell Lung Cancer by Regulating the WTAPP1/WTAP Axis.Current medicinal chemistry · 2024Article
- Identification of a novel target of SETD1A histone methyltransferase and the clinical significance in pancreatic cancer.Cancer science · 2023Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Although histone H3K4 methyltransferase SETD1A is overexpressed in various cancer types, the molecular mechanism underlying its overexpression and its target genes in pancreatic ductal adenocarcinoma (PDAC) remain unclarified. We conducted immunohistochemical staining for SETD1A in 105 human PDAC specimens to assess the relationship between SETD1A overexpression and clinicopathological features. The function and target genes of SETD1A were investigated using human pancreatic cancer cell lines. SETD1A expression was upregulated in 51.4% of patients with PDAC and was an independent prognostic factor associated with shorter disease-free survival after resection (p < 0.05). Knockdown and overexpression of SETD1A showed that SETD1A plays a crucial role in increasing the proliferation and motility of PDAC cells. SETD1A overexpression increased tumorigenicity. RNA sequencing of SETD1A-knockdown cells revealed downregulation of RUVBL1, an oncogenic protein ATP-dependent DNA helicase gene. ChIP analysis revealed that SETD1A binds to the RUVBL1 promoter region, resulting in increased H3K4me3 levels. Knockdown of RUVBL1 showed inhibition of cell proliferation, migration, and invasion of PDAC cells, which are similar biological effects to SETD1A knockdown. High expression of both SETD1A and RUVBL1 was an independent prognostic factor not only for disease-free survival but also for overall survival (p < 0.05). In conclusion, we identified RUVBL1 as a novel downstream target gene of the SETD1A-H3K4me3 pathway. Co-expression of SETD1A and RUVBL1 is an important factor for predicting the prognosis of patients with PDAC.
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