REG3A overexpression suppresses gastric cancer cell invasion, proliferation and promotes apoptosis through PI3K/Akt signaling pathway

被引:21
|
作者
Qiu, Yan-Song [1 ]
Liao, Guang-Jun [2 ]
Jiang, Ning-Ning [2 ]
机构
[1] Yantai Shan Hosp, Dept Gen Surg, Yantai 264000, Shandong, Peoples R China
[2] Yantai Shan Hosp, Dept Bone Tumor, 91 Jiefang Rd, Yantai 264000, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
regenerating islet-derived 3; gastric cancer; invasion; apoptosis; proliferation; phosphatidylinositol; 3; kinase; Akt; PANCREATIC-CANCER; GENE-EXPRESSION; PROTEIN; GROWTH; ADENOCARCINOMA; INVOLVEMENT; HIP/PAP; KINASE; INJURY;
D O I
10.3892/ijmm.2018.3520
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Gastric cancer (GC) is the second most common cause of cancer-related deaths. In recent years some essential factors for resolution were identified, but the clinical trials still lack the effective methods to treat or monitor the disease progression. Regenerating islet-derived 3 (REG3A) is a member of REG protein family. Previous studies have investigated the altered expression of REG3A in various cancers. In this investigtion we aimed at the biological function and the underlying molecular mechanism of REG3A in GC. We found that REG3A was significantly downregulated in GC and closely related with patient prognoses. REG3A overexpression suppressed the invasion and proliferation promoting apoptosis of GC cells. While REG3A knockdown promoted the invasion, and proliferation suppressing apoptosis of GC cells. It was further found that REG3A performed its biological functions mainly through phosphatidylinositol 3 kinase (PI3K)/Akt-GSK3 signaling pathway axis. REG3A may be a promising therapeutic strategy for GC.
引用
收藏
页码:3167 / 3174
页数:8
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