title: RNAi‑mediated knockdown of PRL‑3 inhibits cell invasion and downregulates ERK 1/2 expression in the human gastric cancer cell line, SGC‑7901.
abstract: The deregulated expression of members of the phophatase of regenerating liver (PRL) family is important in the metastatic progression of multiple human cancers; however, the underlying mechanisms are not well understood. Previous studies have demonstrated that PRLs are able to enhance the activation of extracellular signal‑regulated kinase 1/2 (ERK 1/2) in cancer cells, which may contribute to tumor metastasis. However, the effect of PRL‑3 activation in gastric cancer (GC) remains unclear. The present study aimed to investigate whether the downregulation of PRL‑3 by small interfering RNA (siRNA) was able to inhibit cell motility and affect ERK 1/2 expression in human GC. The results demonstrated that the downregulation of PRL‑3 expression by siRNA in human GC cells significantly inhibited cell invasion and migration in vitro; accordingly, inhibition of PRL‑3 also prevented ERK1/2 protein and mRNA expression, and reduced the mRNA level of matrix metalloproteinase‑7 (MMP‑7), the downstream target of ERK 1/2 signaling. Our data demonstrated that RNAi‑mediated downregulation of PRL‑3 expression leads to potent antitumor activity in human GC. Furthermore, ERK 1/2 and MMP‑7 may contribute to the carcinogenesis and development of human GC in combination with PRL‑3.
authors.affiliation: Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Cao
authors.forename: Yi
authors.initials: Y
authors.lastname: Tu
authors.forename: Jinhong
authors.initials: J
authors.lastname: Mei
authors.forename: Zhengrong
authors.initials: Z
authors.lastname: Li
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Jie
authors.forename: Shan
authors.initials: S
authors.lastname: Xu
authors.forename: Linlin
authors.initials: L
authors.lastname: Xu
authors.forename: Shanshan
authors.initials: S
authors.lastname: Wang
authors.forename: Yifeng
authors.initials: Y
authors.lastname: Xiong
mesh_terms: D045744:Cell Line, Tumor; D002465:Cell Movement; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D020783:Matrix Metalloproteinase 7 / Q000235:genetics / Q000378:metabolism; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D017027:Protein Tyrosine Phosphatases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology
chemical_list: D009363:Neoplasm Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; C484730:PTP4A3 protein, human; D017027:Protein Tyrosine Phosphatases; D020783:Matrix Metalloproteinase 7