ArticleThoracic cancer2021
Histone methyltransferase SETD1A participates in lung cancer progression.
Article in Thoracic cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- Case Report: Familial Cold Autoinflammatory Syndrome With Double Variant inCase reports in medicine · 2026Article
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer.Oncology research · 2026Review
- LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Cell cycle dependent methylation of Dam1 contributes to kinetochore integrity and faithful chromosome segregation.PLoS genetics · 2025Article
- Potential mechanism of circKIAA1429 accelerating the progression of hepatocellular carcinoma.Infectious agents and cancer · 2025Article
- 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
- Expanding the coverage of regulons from high-confidence prior knowledge for accurate estimation of transcription factor activities.Nucleic acids research · 2023Article
- SETD1A-mediated H3K4me3 methylation upregulates lncRNA HOXC-AS3 and the binding of HOXC-AS3 to EP300 and increases EP300 stability to suppress the ferroptosis of NSCLC cells.Thoracic cancer · 2023Article
- FOXQ1 recruits the MLL complex to activate transcription of EMT and promote breast cancer metastasis.Nature communications · 2022Article
- SETD1A promotes the proliferation and glycolysis of nasopharyngeal carcinoma cells by activating the PI3K/Akt pathway.Open medicine (Warsaw, Poland) · 2022Article
- SETD1A-SOX2 axis is involved in tamoxifen resistance in estrogen receptor α-positive breast cancer cells.Theranostics · 2022Article
- Histone methyltransferase SETD1A participates in lung cancer progression.Thoracic cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer-related death worldwide, with an estimated 1.2 million deaths each year. Despite advances in lung cancer treatment, 5-year survival rates are lower than ~15%, which is attributes to diagnosis limitations and current clinical drug resistance. Recently, more evidence has suggested that epigenome dysregulation is associated with the initiation and progress of cancer, and targeting epigenome-related molecules improves cancer symptoms. Interestingly, some groups reported that the level of methylation of histone 3 lysine 4 (H3K4me3) was increased in lung tumors and participated in abnormal transcriptional regulation. However, a mechanistic analysis is not available. In this report, we found that the SET domain containing 1A (SETD1A), the enzyme for H3K4me3, was elevated in lung cancer tissue compared to normal lung tissue. Knockdown of SETD1A in A549 and H1299 cells led to defects in cell proliferation and epithelial-mesenchymal transition (EMT), as evidenced by inhibited WNT and transforming growth factor β (TGFβ) pathways, compared with the control group. Xenograft assays also revealed a decreased tumor growth and EMT in the SETD1A silenced group compared with the control group. Mechanistic analysis suggested that SETD1A might regulate tumor progression via several critical oncogenes, which exhibited enhanced H3K4me3 levels around transcriptional start sites in lung cancer. This study illustrates the important role of SETD1A in lung cancer and provides a potential drug target for treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.