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Sci Rep. 2016 Jul 5;6:29385. doi: 10.1038/srep29385.

Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells.

Author information

1
Department of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung, Taiwan.
2
Department of Obstetrics and Gynecology, School of Medicine, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
3
School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
4
Division of Pediatric Surgery, Department of Surgery, Children's Hospital of China Medical University, Taichung, Taiwan.
5
School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
6
Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
7
Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
8
School of Medicine, Tzu Chi University, Hualien, Taiwan.
9
Division of Nephrology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan.
10
Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
11
Clinical laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan.

Abstract

Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increased PTX3 expression was significantly associated with tumor grade (P < 0.011) and differentiation (P < 0.019). Knocking down PTX3 with lentivirus-mediated small hairpin RNA (shRNA) in cervical cancer cell lines resulted in inhibited cell viability, diminished colony-forming ability, and induced cell cycle arrest at the G2/M phase of the cell cycle, along with downregulated expression of cyclin B1, cdc2, and cdc25c, and upregulated expression of p-cdc2, p-cdc25c, p21, and p27. Furthermore, knockdown of PTX3 significantly decreased the potential of migration and invasion of cervical cancer cells by inhibiting matrix metalloproteidase-2 (MMP-2), MMP-9, and urokinase plasminogen activator (uPA). Moreover, in vivo functional studies showed PTX3-knockdown in mice suppressed tumorigenicity and lung metastatic potential. Conversely, overexpression of PTX3 enhanced proliferation and invasion both in vitro and in vivo. Our results demonstrated that PTX3 contributes to tumorigenesis and metastasis of human cervical cancer cells. Further studies are warranted to demonstrate PTX3 as a novel therapeutic biomarker for human cervical cancer.

PMID:
27377307
PMCID:
PMC4932528
DOI:
10.1038/srep29385
[Indexed for MEDLINE]
Free PMC Article

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