Abstract
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.
Highlights
Inhibitor of growth 5 (ING5) belongs to the encoding protein of Class II tumor suppressor gene because its inactivation results from frequent genetic and epigenetic alterations
In line with other reports [12, 13], we found that ING5 overexpression suppressed cell proliferation, tumor growth, glucose and lipid metabolism, and induced cell cycle arrest, apoptosis, senescence, and autophagy of ovarian cancer cells, even highly-invasive or paclitaxelresistant ones
ING5 overexpression resulted in less spindle-like fibroblastic structures and smaller nucleus with N-cadherin hypoexpression and E-cadherin overexpression, indicating that ING5 inhibited cell migration and invasion by reversing epithelial-mesenchymal transition (EMT) process
Summary
Inhibitor of growth 5 (ING5) belongs to the encoding protein of Class II tumor suppressor gene because its inactivation results from frequent genetic and epigenetic alterations. It includes LZL (leucine zipper like), NCR (novel conserved region), NLS (nuclear localization signal), and PHD (plant homeo domain) from N-terminal to C-terminal. ING5 was reported to activate the cyclin-dependent kinase inhibitor p21/ waf promoter to induce p21/waf expression, enhance p53 acetylation at Lys-382 and Lys-120 residues, and physically interact with p300, a member of HAT complexes, and p53 in vivo [6]. Aberrant fat accumulation in ING5 transfectants might be attributable to the up-regulatory ADFP expression [13]
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