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Up-regulation of CNDP2 facilitates the proliferation of colon cancer
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....
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035726/ https://www.ncbi.nlm.nih.gov/pubmed/24885395 http://dx.doi.org/10.1186/1471-230X-14-96 |
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author | Xue, Conglong Zhang, Zhenwei Yu, Honglan Yu, Miao Yuan, Kaitao Yang, Ting Miao, Mingyong Shi, Hanping |
author_facet | Xue, Conglong Zhang, Zhenwei Yu, Honglan Yu, Miao Yuan, Kaitao Yang, Ting Miao, Mingyong Shi, Hanping |
author_sort | Xue, Conglong |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4035726 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40357262014-05-29 Up-regulation of CNDP2 facilitates the proliferation of colon cancer Xue, Conglong Zhang, Zhenwei Yu, Honglan Yu, Miao Yuan, Kaitao Yang, Ting Miao, Mingyong Shi, Hanping BMC Gastroenterol Research Article 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. BioMed Central 2014-05-21 /pmc/articles/PMC4035726/ /pubmed/24885395 http://dx.doi.org/10.1186/1471-230X-14-96 Text en Copyright © 2014 Xue et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. |
spellingShingle | Research Article Xue, Conglong Zhang, Zhenwei Yu, Honglan Yu, Miao Yuan, Kaitao Yang, Ting Miao, Mingyong Shi, Hanping Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title | Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title_full | Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title_fullStr | Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title_full_unstemmed | Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title_short | Up-regulation of CNDP2 facilitates the proliferation of colon cancer |
title_sort | up-regulation of cndp2 facilitates the proliferation of colon cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035726/ https://www.ncbi.nlm.nih.gov/pubmed/24885395 http://dx.doi.org/10.1186/1471-230X-14-96 |
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