ArticleCell death & disease2019
Monomethyltransferase SET8 facilitates hepatocellular carcinoma growth by enhancing aerobic glycolysis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- KMT5A-mediated methylation of IRF3 promotes tumor progression through immune suppression.iScience · 2026Article
- Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.Clinical epigenetics · 2025Review
- SUMOylation of SETD8 Promotes Tumor Growth by Methylating and Stabilizing MYC in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Krüppel-like factors in mitochondrial quality control.Frontiers in physiology · 2025Review
- Sirtuin insights: bridging the gap between cellular processes and therapeutic applications.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Mitochondrial sirtuins: Energy dynamics and cancer metabolism.Molecules and cells · 2024Review
- Immune, metabolic landscapes of prognostic signatures for lung adenocarcinoma based on a novel deep learning framework.Scientific reports · 2024Article
- Targeting sirtuins for cancer therapy: epigenetics modifications and beyond.Theranostics · 2024Review
- SET8 is a novel negative regulator of TGF-β signaling in a methylation-independent manner.Scientific reports · 2023Article
- Article
- Polymorphisms in microRNA binding site ofExperimental and therapeutic medicine · 2023Article
- KLF4 transcription factor in tumorigenesis.Cell death discovery · 2023Review
- SETD8 inhibits ferroptosis in pancreatic cancer by inhibiting the expression of RRAD.Cancer cell international · 2023Article
- The implications and prospect of cuproptosis-related genes and copper transporters in cancer progression.Frontiers in oncology · 2023Review
- SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022Review
- Virtual Screening in the Identification of Sirtuins' Activity Modulators.Molecules (Basel, Switzerland) · 2022Review
- KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling.Nature communications · 2022Article
- Histone Lysine Methylation Modification and Its Role in Vascular Calcification.Frontiers in endocrinology · 2022Review
- LncRNA LINC00473 is involved in the progression of invasive pituitary adenoma by upregulating KMT5A via ceRNA-mediated miR-502-3p evasion.Cell death & disease · 2021Article
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most aggressive cancers worldwide. Despite such a public health importance, efficient therapeutic agents are still lacking for this malignancy. Most tumor cells use aerobic glycolysis to sustain anabolic growth, including HCC, and the preference of glycolysis often leads to a close association with poorer clinical outcomes. The histone methyltransferase SET8 plays crucial roles in controlling cell-cycle progression, transcription regulation, and tumorigenesis. However, it remains largely undefined whether SET8 affects the glucose metabolism in HCC. Here, we report that upregulation of SET8 is positively correlated with a poor survival rate in HCC patients. Both in vitro and in vivo studies revealed that SET8 deficiency conferred an impaired glucose metabolism phenotype and thus inhibited the progression of HCC tumors. By contrast, SET8 overexpression aggravated the glycolytic alterations and tumor progression. Mechanistically, SET8 directly binds to and inactivates KLF4, resulting in suppression of its downstream SIRT4. We also provided further evidence that mutations in SET8 failed to restrain the transactivation of SIRT4 by KLF4. Our data collectively uncover a novel mechanism of SET8 in mediating glycolytic metabolism in HCC cells and may provide a basis for targeting SET8 as a therapeutic strategy in HCC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.