Inhibitory Role of Pentraxin-3 in Esophageal Squamous Cell Carcinoma.
BACKGROUND
Esophageal 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).


METHODS
The 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.


RESULTS
PTX3 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).


CONCLUSIONS
This study indicates that PTX3 might play an inhibitory role in ESCC.
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Dan
D
Ma
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Ye
Y
Zong
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Sheng-Tao
ST
Zhu
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Yong-Jun
YJ
Wang
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Peng
P
Li
Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University; National Clinical Research Center for Digestive Diseases; Beijing Digestive Disease Center; Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing 100050, China.
Shu-Tian
ST
Zhang
D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics / Q000502:physiology; D002470:Cell Survival / Q000235:genetics / Q000502:physiology; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D000077277:Esophageal Squamous Cell Carcinoma; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D000683:Serum Amyloid P-Component / Q000235:genetics / Q000378:metabolism*; D023041:Xenograft Model Antitumor Assays; D000099153:Pentraxins
D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins