Up-regulation of CNDP2 facilitates the proliferation of colon cancer
| Autor: | Miao Yu, Honglan Yu, Zhenwei Zhang, Conglong Xue, Ting Yang, Hanping Shi, Mingyong Miao, Kaitao Yuan |
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| Jazyk: | angličtina |
| Předmět: |
Male
Dipeptidases Pathology medicine.medical_specialty Carcinogenesis Colorectal cancer Transplantation Heterologous Poliferation Mice Nude Adenocarcinoma medicine.disease_cause RNA interference Breast cancer Carcinoembryonic antigen Cell Line Tumor medicine Animals Humans Cyclin B1 Aged Cell Proliferation Cyclin Gene knockdown Clinicopathological Characteristics biology Cell growth business.industry Gastroenterology General Medicine Middle Aged medicine.disease digestive system diseases Colon cancer Up-Regulation CNDP2 Gene Expression Regulation Neoplastic Colonic Neoplasms Cancer research biology.protein Female business Research Article |
| Zdroj: | BMC Gastroenterology |
| ISSN: | 1471-230X |
| DOI: | 10.1186/1471-230x-14-96 |
| Popis: | Background Cytosolic nonspecific dipetidase (CN2) belongs to the family of M20 metallopeptidases. It was stated in previous articles that higher expression levels of CN2 were observed in renal cell carcinoma and breast cancer. Our study explored the correlation between CN2 and colon carcinogenesis. Methods We analysed the relationship between 183 patients clinicopathological characteristics and its CN2 expression. To detect the levels of CN2 in colon cancer cell lines and colon cancer tissues by western blot. To verify cell proliferation in colon cancer cells with knockdown of CNDP2 and explore the causes of these phenomena. Results The expression levels of CN2 in clinical colon tumors and colon cancer cell lines were significantly higher than that in normal colon mucosa and colon cell lines. The difference in CN2 levels was associated with tumor location (right- and left-sided colon cancer), but there was no significant association with age, gender, tumor size, tumor grade, tumor stage or serum carcinoembryonic antigen (CEA). Knockdown of CNDP2 inhibited cell proliferation, blocked cell cycle progression and retarded carcinogenesis in an animal model. The signaling pathway through which knockdown of CNDP2 inhibited cell proliferation and tumorigenesis involved in EGFR, cyclin B1 and cyclin E. Conclusions Knockdown of CNDP2 can inhibit the proliferation of colon cancer in vitro and retarded carcinogenesis in vivo. |
| Databáze: | OpenAIRE |
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