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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
High Expression of BCCIP β Can Promote Proliferation of Esophageal Squamous Cell Carcinoma.
Digestive Diseases and Sciences 2017 Februrary
BACKGROUND: BCCIP was originally identified as a BRCA2 interacting protein in humans and Ustilago maydis. It had low expression in some human cancer tissues. However, recent research indicated that many caretaker genes are also necessary for cell viability and their expression could contribute to tumor progression.
AIM: To characterize whether BCCIP is a caretaker gene in esophageal squamous cell carcinoma (ESCC).
METHODS: Western blotting and immunohistochemistry were used to measure the expression of BCCIP β. In vitro studies were used to verify the effects of BCCIP β in Eca109 cells.
RESULTS: Expression of BCCIP β was notably higher in tumor tissues of ESCC and Eca 109 cells. Meanwhile, the immunohistochemistry stain revealed that BCCIP β was positively correlated with clinical pathologic variables such as tumor size and tumor grade, as well as Ki-67, and prompted poor prognosis. In vitro studies such as starvation and refeeding assay along with BCCIP β-shRNA transfection assay demonstrated that BCCIP β expression promoted proliferation of ESCC cells. In addition, BCCIP β downregulation by silencing RNA significantly decreased the rate of colony formation, alleviated cellular apoptosis and increased the chemosensitivity of cisplatin.
CONCLUSIONS: This research first put forward that BCCIP β is an oncogene in human ESCC and contributes to the poor outcome of the deadly disease.
AIM: To characterize whether BCCIP is a caretaker gene in esophageal squamous cell carcinoma (ESCC).
METHODS: Western blotting and immunohistochemistry were used to measure the expression of BCCIP β. In vitro studies were used to verify the effects of BCCIP β in Eca109 cells.
RESULTS: Expression of BCCIP β was notably higher in tumor tissues of ESCC and Eca 109 cells. Meanwhile, the immunohistochemistry stain revealed that BCCIP β was positively correlated with clinical pathologic variables such as tumor size and tumor grade, as well as Ki-67, and prompted poor prognosis. In vitro studies such as starvation and refeeding assay along with BCCIP β-shRNA transfection assay demonstrated that BCCIP β expression promoted proliferation of ESCC cells. In addition, BCCIP β downregulation by silencing RNA significantly decreased the rate of colony formation, alleviated cellular apoptosis and increased the chemosensitivity of cisplatin.
CONCLUSIONS: This research first put forward that BCCIP β is an oncogene in human ESCC and contributes to the poor outcome of the deadly disease.
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