Abstract
Annexin A2 (ANXA2) has been well known to associate with the progress of malignant tumor. However, the biological behavior of ANXA2 in gastric cancer (GC) remains unclear. We made a hypothesis in transcriptome level from TCGA datasets. Then, we used immunohistochemical staining to quantify the expression level of ANXA2 protein in GC tissues compared with adjacent tissues. Quantitative real-time PCR and western blot were used for analyzing ANXA2 expression in human GC (SGC-7901, MKN-45, BGC-823, and AGS) cell lines. We investigated the effect of a lentivirus-mediated knock-down of ANXA2 on the proliferation, invasion and migration of gastric cancer AGS cells. Cell proliferation was examined by MTT and colony formation tests. Cell apoptosis and cycle were measured by flow cytometry. Migration and invasion were detected by transwell assay. We found that high expression of ANXA2 can increase the mobility of cancer cells from TCGA datasets. ANXA2 was upregulated in GC tissues compared with adjacent tissues. AGS cell line displayed significantly higher expression of ANXA2 among the four GC cell lines. In addition, ANXA2 silencing led to a weakened ability of proliferation, invasion, and migration in GC cells; targeting of ANXA2 may be a potential therapeutic strategy for GC patients.
Highlights
Gastric cancer (GC) is the fifth highest incidence malignant tumor in the world and the third dominant cause of cancer death, with a 5-year survival rate of only 20% to 25% worldwide [1, 2]
By analyzing the expression level of Annexin A2 (ANXA2) in The Cancer Genome Atlas (TCGA) database, we found that ANXA2 was highly homogeneously expressed in GC tissues (Figure 1)
We found that the expression level of ANXA2 in patients with distant metastasis (M1) was higher than that in nondistant metastasis patients (M0)
Summary
Gastric cancer (GC) is the fifth highest incidence malignant tumor in the world and the third dominant cause of cancer death, with a 5-year survival rate of only 20% to 25% worldwide [1, 2]. Despite the improvement of therapeutic methods with surgical resection, chemotherapy, radiotherapy, immunotherapeutic strategies, and targeted therapies, invasion and metastasis lead to the poor prognosis of GC patients and have become a significant clinical challenge [3,4,5,6,7]. Finding new molecular markers which are related to metastasis and poor outcome may contribute to affording new insights into diagnostic decision and novel therapies for GC patients. ANXA2 mainly participates in cell membranes formation and takes effect on regulate cytoskeleton. The cytoskeleton changes are common in malignant transformation, adhesion, movement, and metastasis which may promote tumor cell to move [15]. Targeting cancerous cells motility may be important to the treatments. With the development of transcriptomics, analysis of transcriptome sequencing data from real pathological specimens may provide a comprehensive background for us to understand the relationship between ANAX2 and GC cells
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