ArticleJournal of cell communication and signaling2017
Contribution of LATS1 and LATS2 promoter methylation in OSCC development.
Article in Journal of cell communication and signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- LATS kinases and SLUG regulate the transition to advanced stage in aggressive oral cancer cells.Scientific reports · 2022Article
- Hippo in Gastric Cancer: From Signalling to Therapy.Cancers · 2022Review
- Review
- lncRNA H19 facilitates the proliferation and differentiation of human dental pulp stem cells via EZH2-dependent LATS1 methylation.Molecular therapy. Nucleic acids · 2021Article
- KRT84 is a potential tumor suppressor and good prognosis signature of oral squamous cell carcinoma.Bioscience reports · 2020Article
- LATS1/2 kinases trigger self-renewal of cancer stem cells in aggressive oral cancer.Oncotarget · 2019Article
- LATS1 inhibits metastasis and epithelial-mesenchymal transition in head and neck squamous cell carcinoma.International journal of clinical and experimental pathology · 2018Article
- The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway.Cell death and differentiation · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrant DNA methylation of the tumor suppressor genes involved in DNA Damage Response (DDR) signaling and cell cycle regulation may lead to the tumorigenesis. Our purpose here is to analyze the promoter methylation and mRNA expression levels of LATS1 and LATS2 (LATS1/2) genes in OSCC. Promoter methylation status of LATS1/2 genes was evaluated in 70 OSCC paraffin-embedded tissues and 70 normal oral samples, using Methylation Specific PCR (MSP). LATS1/2 mRNA expression profiles were also investigated in 14 OSCC patients and 14 normal samples, using real-time PCR. In both candidate genes, promoter methylation assessment revealed significant relationship between cases and controls (OR = 2.24, 95 % CI = 1.40-3.54, P = 0.001; LATS1 and OR = 15.5, 95%CI = 3.64-64.76, P < 0.001; LATS2). As well as, the evaluation of mRNA expression levels showed decreased expression in OSCC tissues in compare to control tissues. (Mean ± SD 1.74 ± 0.14 in OSCC versus 2.10 ± 0.24 in controls, P < 0.001; LATS1 and Mean ± SD 1.36 ± 0.077 in OSCC versus 1.96 ± 0.096 in controls, P < 0.001; LATS2). To the best our knowledge, this is the first report regarding the down-regulation of LATS1/2 through promoter methylation in OSCC. It is suggested to explore the down-stream transcription factors of both genes for finding the molecular mechanism of this deregulation in OSCC.
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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.