ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Sam68 promotes cellular proliferation and predicts poor prognosis in esophageal squamous cell carcinoma.
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 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- High expression of HNRNPR in ESCA combined withJournal of translational medicine · 2022Article
- A comprehensive study on genome-wide coexpression network of KHDRBS1/Sam68 reveals its cancer and patient-specific association.Scientific reports · 2019Article
- High expression of Sam68 in sacral chordomas is associated with worse clinical outcomes.OncoTargets and therapy · 2017Article
- The p53 status can influence the role of Sam68 in tumorigenesis.Oncotarget · 2016Article
- Sam68 is Overexpressed in Epithelial Ovarian Cancer and Promotes Tumor Cell Proliferation.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
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Abstract
Sam68 (Src-associated in mitosis of 68 kD) is a KH domain RNA-binding protein. The expression of Sam68 was correlated with kinds of tumors. Yet, the expression mechanisms and physiological significance of Sam68 in ESCC remains unclear. In this study, we clarified a potential role of Sam68 in the treatment of ESCC. Western blot and immunohistochemistry (IHC) analysis revealed that the protein level of Sam68 was higher in ESCC tumor tissues and cell lines. In addition, IHC stain revealed that Sam68 was positively correlated with clinical pathologic variables such as tumor grade and tumor invasion. In addition, Sam68 could be an independent prognostic indicator for patients' overall survival. In vitro studies such as starvation and refeeding assay along with Sam68-shRNA transfection assay demonstrated that Sam68 expression promoted proliferation of ESCC cells. And Sam68 downregulation caused decreased rate of cell growth and colony formation. Reasons are associated with growth arrest of cell cycle at G1/S phase. Moreover, our results clarified that Sam68 could promote ESCC cell proliferation via the activation of Akt/GSK-3β pathway. This research indicated that Sam68 might accelerate the cell cycle progression and be considered as a new therapy target in ESCC.
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