ArticleAmerican journal of translational research2019
Depletion of H3K79 methyltransferase Dot1L promotes cell invasion and cancer stem-like cell property in ovarian cancer.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- The 80Journal of microbiology and biotechnology · 2024Article
- The Role of Histone Modification in DNA Replication-Coupled Nucleosome Assembly and Cancer.International journal of molecular sciences · 2023Review
- DOT1 L Regulates Ovarian Cancer Stem Cells by Activating β-catenin Signaling.Molecular cancer research : MCR · 2023Article
- Epigenetic drug library screening reveals targeting DOT1L abrogates NADJournal of pharmaceutical analysis · 2023Article
- The roles of histone modifications in tumorigenesis and associated inhibitors in cancer therapy.Journal of the National Cancer Center · 2022Review
- Histone Methyltransferase DOT1L as a Promising Epigenetic Target for Treatment of Solid Tumors.Frontiers in genetics · 2022Review
- Comprehensive analysis of histone methylation modification regulators for predicting prognosis and drug sensitivity in lung adenocarcinoma.Frontiers in cell and developmental biology · 2022Article
- Article
- Histone Modifying Enzymes in Gynaecological Cancers.Cancers · 2021Review
- Endometriosis and ovarian cancer risk, an epigenetic connection.Annals of translational medicine · 2020Review
- Histone Monoubiquitination in Chromatin Remodelling: Focus on the Histone H2B Interactome and Cancer.Cancers · 2020Review
- DOT1L: a key target in normal chromatin remodelling and in mixed-lineage leukaemia treatment.Epigenetics · 2020Review
- Alterations of cell cycle genes in cancer: unmasking the role of cancer stem cells.Molecular biology reports · 2020Review
- Silencing or inhibition of H3K79 methyltransferase DOT1L induces cell cycle arrest by epigenetically modulating c-Myc expression in colorectal cancer.Clinical epigenetics · 2019Article
- Wnt/β-catenin signalling in ovarian cancer: Insights into its hyperactivation and function in tumorigenesis.Journal of ovarian research · 2019Review
- Reprogramming: identifying the mechanisms that safeguard cell identity.Development (Cambridge, England) · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DOT1-like protein (Dot1L) is the sole methyltransferase for methylation of lysine 79 in histone H3. Dot1L-dependent H3K79 methylation is involved in many biological processes, including telomeric silencing, cell cycle regulation, transcriptional activation and DNA repair. Genome-wide sequencing studies have revealed recurrent deletion and mutations of Dot1L gene in many types of human malignancies including ovarian cancer, however the role of Dot1L in ovarian cancer are largely unknown. To demonstrate the role of Dot1L in ovarian cancer, the expression of Dot1L was knocked out in ovarian cancer cells using CRISPR/Cas9 technology in the present study. Dot1L loss showed minimal effect on cell growth, but significantly promoted cell invasion and induced cancer stem-like cell property in ovarian cancer cells. Mechanistically, loss of Dot1L downregulated the expression of tight junction makers E-Cadherin and TJP1 and upregulated the expression of ALDH1A1 through Wnt signaling activation. Our data indicate potential tumor suppressor function of Dot1L in ovarian cancer, which is correlated with observed deletion of Dot1L gene in ovarian cancer patients, further study is granted to elucidate the function of Dot1L in tumorigenesis and progression in ovarian cancer.
Indexed as
Identifiers
30899413PMC6413254W2989322873What 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.