Connexin32 inhibits gastric carcinogenesis through cell cycle arrest and altered expression of p21Cip1 and p27Kip1 |
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Authors: | Hyang Jee Su-Hyung Lee Jun-Won Park Bo-Ram Lee Ki-Taek Nam Dae-Yong Kim |
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Affiliation: | 1.Department of Veterinary Pathology and Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea;2.Nashville Department of Veterans Affairs Medical Center, Vanderbilt University School of Medicine, Nashville, Tennessee, 37232-2733, USA |
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Abstract: | Gap junctions and their structural proteins, connexins (Cxs), have been implicated in carcinogenesis. To explore the involvement of Cx32 in gastric carcinogenesis, immunochemical analysis of Cx32 and proliferation marker Ki67 using tissue-microarrayed human gastric cancer and normal tissues was performed. In addition, after Cx32 overexpression in the human gastric cancer cell line AGS, cell proliferation, cell cycle analyses, and p21Cip1 and p27Kip1 expression levels were examined by bromodeoxyuridine assay,flow cytometry, real-time RT-PCR, and western blotting. Immunohistochemical study noted a strong inverse correlation between Cx32 and Ki67 expression pattern as well as theirlocation. In vitro, overexpression of Cx32 in AGS cells inhibited cell proliferation significantly. G1 arrest, up-regulation of cell cycle-regulatory proteins p21Cip1 and p27Kip1 was also found at both mRNA and protein levels. Taken together, Cx32 plays some roles in gastric cancer development by inhibiting gastric cancer cell proliferation through cell cycle arrest and cell cycle regulatory proteins. [BMB Reports 2013; 46(1): 25-30] |
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Keywords: | AGS cells Cell cycle distribution Cell proliferation Connexin32 Gastric cancer |
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