Abstract
Circular RNAs (circRNAs), a new class of endogenous non-coding RNAs, have recently been known to play critical roles in various cellular biological processes, including tumorigenesis, in which they act as an miRNA sponge that regulates gene expression. Thus, revealing the functions of circRNAs in carcinogenesis and cancer development has been of great interest. However, their expression and functions in gastric cancer (GC) development are still largely unknown. Therefore, the present study aimed to identify novel deregulated circRNAs in GC and reveal their biological functions and molecular mechanisms in GC. Quantitative real-time PCR (qRT-PCR) was performed to measure the expression levels of circRNAs in GC tissues, cell lines, and plasma. The MTT assay, colony formation assay, transwell assay, and tumor xenografts in vivo were used to evaluate the effects of circRNAs on the proliferation and invasion of GC. The abovementioned methods coupled with Western blotting were used to investigate the molecular mechanisms. The current study showed that hsa_circ_0000673 was significantly down-regulated in GC. Overexpression of hsa_circ_0000673 inhibited the proliferation and invasion of GC cells. In contrast, hsa_circ_0000673 down-regulation promoted the proliferation and invasion of GC cells. Further studies revealed that hsa_circ_0000673 targetted miR-532-5p and up-regulated the expression of RUNX3. The present study showed that hsa_circ_0000673 was decreased in GC and it exerted tumor-suppressing effects by targetting miR-532-5p and up-regulating RUNX3 expression level. Hsa_circ_0000673 may be a promising diagnosis biomarker and therapeutic target in GC.
Highlights
Gastric cancer (GC) is a common malignant tumor with the fourth highest occurrence amongst all cancers and is the second leading cause of cancer-related deaths worldwide [1,2]
We found that hsa circ 0000673, hsa circ 0009172, and hsa circ 0074854 were all significantly down-regulated in GC tissues, compared with those in non-tumor tissues (Figure 1A)
C and Supplementary Figure S1A,B, the expression levels of hsa circ 0000673 and hsa circ 0074854 were significantly down-regulated in the GC cell lines and GC tissue samples than in the normal human gastric epithelial cell line GES-1 and the normal gastric epithelial cells samples, respectively. Both in vitro and in vivo, there was no significant difference in the expression level of hsa circ 0009172 between GC and normal cells (Supplementary Figure S1C,D)
Summary
Gastric cancer (GC) is a common malignant tumor with the fourth highest occurrence amongst all cancers and is the second leading cause of cancer-related deaths worldwide [1,2]. Many Asian countries have high incidence of GC, especially China and Japan [3,4]. From 2009 to 2011, 679100 patients were diagnosed with GC in China, of which 498000 died [4]. The occurrence and development of GC are complex biological processes accompanied by the activation of oncogenes or dysregulation of tumor suppressor genes [6,7,8,9,10]. The molecular mechanism underlying gastric carcinogenesis has not been fully understood. Further elucidation on the molecular mechanism underlying GC development is beneficial in identifying new diagnostic and therapeutic targets
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