ArticleJournal of Cancer2019
SYT12 plays a critical role in oral cancer and may be a novel therapeutic target.
Article in Journal of Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- SPOP-dependent destabilization of SYT12 in a GSK-3β-dependent manner in papillary thyroid cancer cells.Clinical and experimental medicine · 2025Article
- Integration of bioinformatics and cellular experiments unveils the role of SYT12 in gastric cancer.BMC cancer · 2024Article
- Correlations of mInternational journal of general medicine · 2024Article
- Establishment and assessment of an oral squamous cell carcinoma N7-methylguanosine methyltransferase associated microRNA prognostic model.Journal of Cancer · 2024Article
- Article
- Chromosome-level genome assembly and population genomics of Mongolian racerunner (Eremias argus) provide insights into high-altitude adaptation in lizards.BMC biology · 2023Article
- Potential roles of synaptotagmin family members in cancers: Recent advances and prospects.Frontiers in medicine · 2022Review
- Tumor Suppressive Circular RNA-102450: Development of a Novel Diagnostic Procedure for Lymph Node Metastasis from Oral Cancer.Cancers · 2021Article
- The dysregulated expression and functional effect of CaMK2 in cancer.Cancer cell international · 2021Review
- SYT12 is a novel oncogene that promotes thyroid carcinoma progression and metastasis.Journal of Cancer · 2021Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptotagmin12 (SYT12) has been well characterized as the regulator of transmitter release in the nervous system, however the relevance and molecular mechanisms of SYT12 in oral squamous cell carcinoma (OSCC) are not understood. In the current study, we investigated the expression of SYT12 and its molecular biological functions in OSCC by quantitative reverse transcriptase polymerase chain reaction, immunoblot analysis, and immunohistochemistry. SYT12 were up-regulated significantly in OSCC-derived cell lines and primary OSCC tissue compared with the normal counterparts (P<0.05) and the SYT12 expression levels were correlated significantly with clinical indicators, such as the primary tumoral size, lymph node metastasis, and TNM stage (P<0.05). SYT12 knockdown OSCC cells showed depressed cellular proliferation, migration, and invasion with cell cycle arrest at G1 phase. Surprisingly, we found increased calcium/calmodulin-dependent protein kinase 2 (CAMK2) inhibitor 1 (CAMK2N1) and decreased CAMK2-phosphorylation in the knockdown cells. Furthermore, treatment with L-3, 4-dihydroxyphenylalanine (L-dopa), a drug approved for Parkinson's disease, led to down-regulation of SYT12 and similar phenotypes to SYT12 knockdown cells. Taken together, we concluded that SYT12 plays a significant role in OSCC progression via CAMK2N1 and CAMK2, and that L-dopa would be a new drug for OSCC treatment through the SYT12 expression.
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