The roles of ING5 expression in ovarian carcinogenesis and subsequent progression: a target of gene therapy
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Hua-Chuan Zheng1, Shuang Zhao1, Yang Song2 and Xiao-Qing Ding1
1Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China
2Department of Pathology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121001, China
Hua-Chuan Zheng, email: [email protected]
Keywords: ovarian cancer, ING5, pathogenesis, progression, prognosis
Received: July 14, 2017 Accepted: September 21, 2017 Published: October 19, 2017
Here, we found that ING5 overexpression suppressed cell viability, glucose metabolism, migration, invasion and epithelial-mesenchymal transition, and induced cell arrest, apoptosis, senescence, autophagy and fat accumulation in ovarian cancer cells. ING5-mediated chemoresistance was positively linked to apoptotic resistance and chemoresistance-related gene expression. ING5 overexpression suppressed tumor growth of ovarian cancer by decreasing proliferation, and inducing apoptosis and autophagy. ING5 mRNA level was lower in ovarian cancer than normal ovary, and borderline than benign tumors (p < 0.05), and negatively correlated with vascular invasion, lymphatic invasion and FIGO staging of ovarian cancer (p < 0.05). ING5 protein was less expressed in primary cancer than normal ovary (p < 0.05). There was a negative correlation between ING5 mRNA expression and the overall or progression-free survival time of the cancer patients with Grade 2, Grade 3, and stage I cancer (p < 0.05). Immunohistochemically, ING5 was less expressed in serous and mucinous adenocarcinoma than miscellaneous subtypes, and positively correlated with dedifferentiation and ki-67 expression of ovarian cancer (p < 0.05). These data suggested that down-regulated ING5 expression might be involved in ovarian carcinogenesis possibly by suppressing aggressive phenotypes, including proliferation, tumor growth, migration, invasion, and anti-apoptosis.
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