- Author:
Dan MA
1
,
2
,
3
,
4
;
Ye ZONG
1
;
Sheng-Tao ZHU
1
;
Yong-Jun WANG
1
;
Peng LI
1
;
Shu-Tian ZHANG
1
;
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; genetics; physiology; C-Reactive Protein; genetics; metabolism; Carcinoma, Squamous Cell; metabolism; pathology; Cell Line, Tumor; Cell Proliferation; genetics; physiology; Cell Survival; genetics; physiology; Esophageal Neoplasms; metabolism; pathology; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Serum Amyloid P-Component; genetics; metabolism; Xenograft Model Antitumor Assays
- From: Chinese Medical Journal 2016;129(18):2233-2240
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDEsophageal cancer is the sixth leading cause of cancer-related death worldwide. Pentraxin-3 (PTX3) is a member of the PTX superfamily. Here, we investigated the role of PTX3 in esophageal squamous cell carcinoma (ESCC).
METHODSThe effect of PTX3 on ESCC cell proliferation, colony formation, apoptosis, migration, and invasion was investigated using cell viability assays, colony formation assays, flow cytometry, and migration and invasion assays. The effect of PTX3 on the tumorigenicity of ESCC in vivo was investigated with xenograft studies in nude mice.
RESULTSPTX3 overexpression in ESCC cells reduced cellular proliferation and colony formation (P < 0.05) and increased the rate of apoptosis (P < 0.05). PTX3 expression had no significant effect on the migratory or invasive potential of ESCC cells. In our mouse model of human ESCC, we achieved 100% successful tumor establishment. Compared with the control and empty vector-expressing groups, the PTX3-expressing group formed significantly smaller tumors (P < 0.05).
CONCLUSIONSThis study indicates that PTX3 might play an inhibitory role in ESCC.