Aim: To investigate expression of stem cell marker Musashi-1 (Msi-1) in relationship to tumorigenesis and progression of intestinal-type gastric cancer (GC).
Methods: Endoscopic biopsy specimens and surgical specimens were obtained, including 54 cases of intestinal-type GC, 41 high-grade intraepithelial neoplasia, 57 low-grade intraepithelial neoplasia, 31 intestinal metaplasia, and 36 normal gastric mucosa. Specimens were fixed in 10% paraformaldehyde, conventionally dehydrated, embedded in paraffin, and sliced in 4-μm-thick serial sections. Two-step immunohistochemical staining was used to detect Msi-1 and proliferating cell nuclear antigen (PCNA) expression. Correlation analysis was conducted between Msi-1 and PCNA expression. The relationship between Msi-1 expression and clinicopathological parameters of GC was analyzed statistically.
Results: There were significant differences in Msi-1 and PCNA expression in different pathological tissues (χ² = 15.37, P < 0.01; χ² = 115.36, P < 0.01). Msi-1 and PCNA-positive cells were restricted to the isthmus of normal gastric glands. Expression levels of Msi-1 and PCNA in intestinal metaplasia were significantly higher than in normal mucosa (U = 392.0, P < 0.05; U = 40.50, P < 0.01), whereas there was no significant difference compared to low or high-grade intraepithelial neoplasia. Msi-1 and PCNA expression in intestinal-type GC was higher than in high-grade intraepithelial neoplasia (U = 798.0, P < 0.05; U = 688.0, P < 0.01). There was a significantly positive correlation between Msi-1 and PCNA expression (r(s) = 0.20, P < 0.01). Msi-1 expression in GC tissues was correlated with their lymph node metastasis and tumor node metastasis stage (χ² = 12.62, P < 0.01; χ² = 11.24, P < 0.05), but not with depth of invasion and the presence of distant metastasis.
Conclusion: Msi-1-positive cells may play a key role in the early events of gastric carcinogenesis and may be involved in invasion and metastasis of GC.
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http://dx.doi.org/10.3748/wjg.v19.i39.6637 | DOI Listing |
Adv Clin Exp Med
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Department of Head and Neck Oncology, Shaanxi Provincial Cancer Hospital Affiliated to Xi'an Jiaotong University, China.
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Department of Gastroenterological Surgery I, Hokkaido University Graduate School of Medicine, N15 W7 Kita-Ku, Sapporo, Hokkaido, 060-8638, Japan.
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Department of Medical Pharmacology, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
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Engineering Technological Center of Mushroom Industry, Minnan Normal University, Zhangzhou, Fujian 363000, People's Republic of China.
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Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, 15, 816 Beon-gil, Jinjudaero, Jinju, 52727, Republic of Korea.
Chronic kidney disease is defined as a progressive loss of kidney function associated with impaired recovery after acute kidney injury. Renal ischemia-reperfusion (IR) induces oxidative stress and inflammatory responses leading to severe tissue damage, where incomplete or maladaptive repair accelerates renal fibrosis and aging. To investigate the role of the purinergic P2Y2 receptor (P2Y2R) in these processes, we used P2Y2R knockout (KO) mice subjected to IR.
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