ArticleOncology letters2019
MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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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.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- MRG15 alternative splicing regulates CDK1 transcriptional activity in mouse cell senescence and myocardial regeneration.Communications biology · 2025Article
- Integrative Multi-Omics Approach for Improving Causal Gene Identification.Genetic epidemiology · 2025Article
- Structural and functional insights into the epigenetic regulator MRG15.Acta pharmacologica Sinica · 2024Review
- PRR11 unveiled as a top candidate biomarker within the RBM3-regulated transcriptome in pancreatic cancer.The journal of pathology. Clinical research · 2022Article
- SLC25A10 performs an oncogenic role in human osteosarcoma.Oncology letters · 2020Article
- TRIM11 facilitates chemoresistance in nasopharyngeal carcinoma by activating the β-catenin/ABCC9 axis via p62-selective autophagic degradation of Daple.Oncogenesis · 2020Article
- THAP7 promotes cell proliferation by regulating the G1/S phase transition via epigenetically silencing p21 in lung adenocarcinoma.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the promoter of MORF4L1 was identified to be significantly higher in tumour cells than in normal cells. The ectopic expression of MORF4L1 was also revealed to inhibit cell proliferation, colony formation, migration and invasion in NPC, whereas the knockdown of MORF4L1 promoted cell proliferation, colony formation, migration and invasion. Mechanistically, the present study demonstrated that MORF4L1 functions as a tumour suppressor by increasing p21 and E-cadherin levels. These findings may be useful novel targets for treating patients with NPC.
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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 OpenQuestion graph.