ArticleOncology reports2018
SET7/9 promotes hepatocellular carcinoma progression through regulation of E2F1.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Identification of Gαi1 as a key regulator of tumor progression in nasopharyngeal carcinoma.Discover oncology · 2025Article
- SETD7-mediated H3K4me1 activates ALDH1A3 to drive ferroptosis resistance in esophageal squamous cell carcinoma.Cell death & disease · 2025Article
- E2F1 Facilitates the Proliferation and Stemness of Gastric Cancer Cells by Activating CDC25B Transcription and Modulating the MAPK Pathway.Biochemical genetics · 2025Article
- Lysine methyltransferase SETD7 in cancer: functions, molecular mechanisms and therapeutic implications.Molecular biology reports · 2025Review
- MCM8 promotes NR4A1-mediated E2F1 transcription and facilitates renal cell carcinoma through enhancing aerobic glycolysis.Cell biology and toxicology · 2025Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Actin like 6A is a prognostic biomarker and associated with immune cell infiltration in cancers.Discover oncology · 2024Article
- SETD7 Promotes Cell Proliferation and Migration via Methylation-mediated TAF7 in Clear Cell Renal Cell Carcinoma.International journal of biological sciences · 2024Article
- The methyltransferase N6AMT1 participates in the cell cycle by regulating cyclin E levels.PloS one · 2024Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- Long non-coding RNA CDKN2B-AS1 promotes hepatocellular carcinoma progressionWorld journal of gastrointestinal oncology · 2023Article
- SNHG15 enhances cisplatin resistance in lung adenocarcinoma by affecting the DNA repair capacity of cancer cells.Diagnostic pathology · 2023Article
- The role of SET domain containing lysine methyltransferase 7 in tumorigenesis and development.Cell cycle (Georgetown, Tex.) · 2023Review
- [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023Review
- Article
- LINC00265 Promotes Metastasis and Progression of Hepatocellular Carcinoma by Interacting with E2F1 at The Promoter ofCell journal · 2022Article
- Lysine methyltransferase inhibitors: where we are now.RSC chemical biology · 2022Review
- LINC00852 Regulates Cell Proliferation, Invasion, Migration and Apoptosis in Hepatocellular CarcinomaCellular and molecular bioengineering · 2022Article
- Positive regulation of ataxia-telangiectasia-mutated protein (ATM) by E2F transcription Factor 1 (E2F-1) in cisplatin-resistant nasopharyngeal carcinoma cells.World journal of surgical oncology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide. Histone‑lysine N‑methyltransferase SET7/9 is a protein lysine monomethylase that methylates histone H3K4 as well as various non‑histone proteins. Deregulation of SET7/9 is frequently detected in human cancers. However, the role of SET7/9 in HCC development remains unclear. In the present study, upregulation of SET7/9 and E2F transcription factor 1 (E2F1) expression was detected in 68 samples of HCC tissues compared with these levels noted in the paired healthy liver samples. The expression levels of SET7/9 and E2F1 were significantly correlated with pathological stage and tumor size. Subcellular fractionation and co‑immunoprecipitation analyses revealed protein‑protein interaction between SET7/9 and E2F1 in the cytoplasm of HCC cells. Silencing of SET7/9, as well as treatment with 5'‑deoxy‑5'‑methylthioadenosine (MTA), a protein methylation inhibitor, led to reduced E2F1 protein abundance in HCC cells. Using Cell Counting Kit‑8 (CCK‑8) assay, Transwell migration assay and wound healing assay, significantly decreased cell proliferation, migration and invasion were observed in cells exhibiting downregulation of SET7/9 and E2F1 expression, as well as in wild‑type HCC cells treated with MTA. Furthermore, SET7/9 downregulation and MTA treatment resulted in reduced expression of downstream targets of E2F1, including cyclin A2, cyclin E1 and CDK2. In conclusion, the present study revealed an oncogenic function of SET7/9 in HCC and demonstrated that SET7/9 may be responsible for alterations in the proliferative ability, aggressiveness and invasive/metastatic potential of HCC cells through post‑translational regulation of E2F1.
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