ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
SYF2 is upregulated in human epithelial ovarian cancer and promotes cell proliferation.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Editorial: RNA machines.Frontiers in genetics · 2023Article
- Discovering Breast Cancer Biomarkers Candidates through mRNA Expression Analysis Based on The Cancer Genome Atlas Database.Journal of personalized medicine · 2022Article
- Genome-wide comparison andFrontiers in genetics · 2022Article
- Hsa-circ_0000064 accelerates the malignant progression of gastric cancer via sponging microRNA-621.The Kaohsiung journal of medical sciences · 2021Article
- Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer.Technology in cancer research & treatment · 2019Article
- Overexpression of SYF2 promotes cell proliferation and correlates with poor prognosis in human breast cancer.Oncotarget · 2017Article
- Overexpression of tumor necrosis factor receptor-associated protein 1 (TRAP1) are associated with poor prognosis of epithelial ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
SYF2 is reported to be as a cell cycle regulator at the G1/S transition and encodes a nuclear protein that interacts with cyclin-D-type binding protein 1. In our study, we investigated the role of SYF2 in human epithelial ovarian cancer (EOC) progression. Western blot and immunohistochemistry analysis displayed that SYF2 was overexpressed in EOC tissues and EOC cell lines. In addition, the immunoreactivity of SYF2 was positively correlated with tumor grade and Ki-67 expression. In vitro, serum starvation-refeeding experiment and SYF2-siRNA transfection assay demonstrated that the expression of SYF2 was promoted in the proliferative progression of EOC cells, while knockdown of SYF2 expression decreased and inhibited cell growth rate of EOC cells. With all the results, we support that SYF2 might contribute to EOC progression via modulation of proliferation in EOC cells and would provide a novel therapeutic target of human EOC.
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