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01.12.2014 | Research article | Ausgabe 1/2014 Open Access

BMC Gastroenterology 1/2014

Up-regulation of CNDP2 facilitates the proliferation of colon cancer

Zeitschrift:
BMC Gastroenterology > Ausgabe 1/2014
Autoren:
Conglong Xue, Zhenwei Zhang, Honglan Yu, Miao Yu, Kaitao Yuan, Ting Yang, Mingyong Miao, Hanping Shi
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1471-230X-14-96) contains supplementary material, which is available to authorized users.
Conglong Xue, Zhenwei Zhang, Honglan Yu contributed equally to this work.

Competing interests

The authors have no competing interests to declare.

Authors’ contributions

HPS, MY and CLX have conceived and designed the experiments, as well as have been involved in drafting the manuscript. CLX and ZWZ have performed the experiments. HLY and MY have participated inclinical data and information collection. CLX, KTY and TY have analyzed the date. All authors read and approved the final manuscript.

Abstract

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.
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