High expression of PRL-3 can promote growth of gastric cancer and exhibits a poor prognostic impact on patients.
High expression of PRL-3 had been implicated in lymph node metastasis of gastric cancer. In the present study, we detected the expression of PRL-3 in primary gastric cancer tissue, and evaluated its role in gastric cancer growth and the prognostic impact on patients. PRL-3 phosphatase expression was measured in 137 gastric tumor samples by using the immunohistochemistry method, and the overall survival rate was compared between the patients with high PRL-3 expression (n = 85) and those with moderate or low PRL-3 expression (n = 52). RNA interference, mediated by recombinant lentivirus expressing artificial PRL-3 miRNA, was used to knockdown PRL-3 expression in SGC7901 cell line. MTT assay and animal experiment were conducted to determine the role of PRL-3 in the proliferation of SGC7901 cells and tumor growth. PRL-3 expression was more frequently detected in tumors with a diameter >40 mm and in advanced stages. Furthermore, the overall survival rate of high PRL-3 expression was significantly lower than that of moderate or low PRL-3 expression (P < 0.001), and multivariate analysis showed that PRL-3 expression level independently influences the survival of patients (P = 0.024). Importantly, knockdown of PRL-3 significantly suppressed the proliferation of SGC7901 cells and slowed the tumor growth compared with controls (P < 0.05). PRL-3 is associated with gastric cancer progression. High PRL-3 expression in the primary lesion had a negative impact on prognosis. PRL-3 plays a key role in the control of gastric cancer growth. PRL-3 should be considered as a potential therapeutic target and a prognostic factor.
Wang
Zhao
Z
Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Cai
Shi-Rong
SR
He
Yu-Long
YL
Zhan
Wen-Hua
WH
Chen
Chuang-Qi
CQ
Cui
Ji
J
Wu
Wen-Hui
WH
Wu
Hui
H
Song
Wu
W
Zhang
Chang-Hua
CH
Peng
Jian-Jun
JJ
Huang
Xiao-Hui
XH
D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000556:secondary; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D017209:Apoptosis; D014408:Biomarkers, Tumor / Q000378:metabolism*; D015153:Blotting, Western; D002454:Cell Differentiation; D049109:Cell Proliferation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007124:Immunoenzyme Techniques; D016086:Lentivirus / Q000235:genetics; D008207:Lymphatic Metastasis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000494:pharmacology; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009367:Neoplasm Staging; D011379:Prognosis; D017027:Protein Tyrosine Phosphatases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D015996:Survival Rate; D055815:Young Adult
D014408:Biomarkers, Tumor; D035683:MicroRNAs; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; C484730:PTP4A3 protein, human; D017027:Protein Tyrosine Phosphatases