Gastric cancer (GC) is a major cause of cancer-related deaths worldwide, and has a low survival rate, low cure rate, high recurrence rate, and poor prognosis. Recent studies have indicated that circular RNAs (circRNAs) have important functions in the occurrence and progression of GC. Studies on circ-NOTCH1, which was shown to be highly expressed in GC, have indicated that miR-637 binds to circ-NOTCH1 at multiple sites, and a dual-luciferase reporter gene assay further confirmed that miR-637 indeed targeted circ-NOTCH1 and Apelin. Circ-NOTCH1 and Apelin are highly expressed in GC cells and tissues, whereas the expression of miR-637 is reduced. Circ-NOTCH1 and miR-637 do not regulate each other's expression levels, but circ-NOTCH1significantly upregulates the expression of the miR-637 target gene Apelin, whereas miR-637 inhibites the expression of Apelin. Examination of GC cells showed that circ-NOTCH1 enhances cell proliferation and invasiveness, and reduces cell apoptosis; these effects were reversed by miR-637, which could terminate the above effects of circ-NOTCH1. When co-transfected with the circ-NOTCH1 overexpression plasmid and Apelin siRNAs, there were no obvious changes to the levels of cell proliferation, apoptosis, or invasiveness. Therefore, in GC cells, circ-NOTCH1 inhibits the transcriptional activity of miR-637, thereby upregulating the expression of its target gene Apelin and regulating cell proliferation, apoptosis, and invasiveness. This finding provides more experimental evidence for the function of circRNA in GC.

中文翻译：

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circ-NOTCH1充当miR-637的海绵，并影响其靶基因Apelin的表达以调节胃癌细胞的生长。

胃癌（GC）是全球范围内与癌症相关的死亡的主要原因，其生存率低，治愈率低，复发率高且预后不良。最近的研究表明，环状RNA（circRNA）在GC的发生和发展中具有重要的功能。对circ-NOTCH1的研究表明在GC中高表达，表明miR-637在多个位点与circ-NOTCH1结合，并且双荧光素酶报告基因检测进一步证实miR-637确实靶向circ-NOTCH1和阿佩林。Circ-NOTCH1和Apelin在GC细胞和组织中高度表达，而miR-637的表达则降低。Circ-NOTCH1和miR-637不调节彼此的表达水平，但是circ-NOTCH1显着上调了miR-637目标基因Apelin的表达，而miR-637抑制Apelin的表达。对GC细胞的检查表明，circ-NOTCH1增强细胞增殖和侵袭性，并减少细胞凋亡。这些作用被miR-637逆转，可以终止circ-NOTCH1的上述作用。当与circ-NOTCH1过表达质粒和Apelin siRNA共转染时，细胞增殖，凋亡或侵袭性水平没有明显变化。因此，在GC细胞中，circ-NOTCH1抑制miR-637的转录活性，从而上调其靶基因Apelin的表达并调节细胞增殖，凋亡和侵袭性。这一发现为circRNA在GC中的功能提供了更多的实验证据。并减少细胞凋亡；这些作用被miR-637逆转，可以终止circ-NOTCH1的上述作用。当与circ-NOTCH1过表达质粒和Apelin siRNA共转染时，细胞增殖，凋亡或侵袭性水平没有明显变化。因此，在GC细胞中，circ-NOTCH1抑制miR-637的转录活性，从而上调其靶基因Apelin的表达并调节细胞增殖，凋亡和侵袭性。这一发现为circRNA在GC中的功能提供了更多的实验证据。并减少细胞凋亡；这些作用被miR-637逆转，可以终止circ-NOTCH1的上述作用。当与circ-NOTCH1过表达质粒和Apelin siRNA共转染时，细胞增殖，凋亡或侵袭性水平没有明显变化。因此，在GC细胞中，circ-NOTCH1抑制miR-637的转录活性，从而上调其靶基因Apelin的表达并调节细胞增殖，凋亡和侵袭性。这一发现为circRNA在GC中的功能提供了更多的实验证据。细胞凋亡或侵袭性。因此，在GC细胞中，circ-NOTCH1抑制miR-637的转录活性，从而上调其靶基因Apelin的表达并调节细胞增殖，凋亡和侵袭性。这一发现为circRNA在GC中的功能提供了更多的实验证据。细胞凋亡或侵袭性。因此，在GC细胞中，circ-NOTCH1抑制miR-637的转录活性，从而上调其靶基因Apelin的表达并调节细胞增殖，凋亡和侵袭性。这一发现为circRNA在GC中的功能提供了更多的实验证据。