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Abstract：
BACKGROUND: Gastric cancer (GC) is considered as one of the most widespread malignancies. Emerging evidence has shown that lncRNAs can function as important oncogenes or tumor suppressors during GC progression.
OBJECTIVE: To investigate the effect and mechanism of lncRNA cancer susceptibility 20 (CASC20) in the proliferation and metastasis of GC cells.
METHODS: Data mining and clinical samples were used to evaluate the expression of CASC20 in GC and adjacent tissues. CASC20 was down-regulated in GC cells by short-interfering RNA. Cell proliferation was evaluated by CCK-8 assay, and cell migration and invasion were detected by wound healing and Transwell assays. The expressions of proteins related to epithelial-mesenchymal transition were detected by western blot assay.
RESULTS: The expression of CASC20 was increased in GC tumor tissues and various GC cell lines. High CASC20 expression was correlated with a high risk of lymphatic metastasis and poor prognosis in GC patients. In vitro assays showed that silencing CASC20 reduced cell proliferation, migration, and invasion in GC cells. Mechanistic studies revealed that CASC20 exhibits oncogenic functions by regulating MEMO1 expression through competitive endogenous binding to miR-143-5p, leading to induction of epithelial-mesenchymal transition.
CONCLUSIONS: Our findings indicate that CASC20 serves as a tumor promoter by regulating metastasis in GC via the miR-143-5p/MEMO1 axis. CASC20 may be a potential therapeutic target for GC.
OBJECTIVE: To investigate the effect and mechanism of lncRNA cancer susceptibility 20 (CASC20) in the proliferation and metastasis of GC cells.
METHODS: Data mining and clinical samples were used to evaluate the expression of CASC20 in GC and adjacent tissues. CASC20 was down-regulated in GC cells by short-interfering RNA. Cell proliferation was evaluated by CCK-8 assay, and cell migration and invasion were detected by wound healing and Transwell assays. The expressions of proteins related to epithelial-mesenchymal transition were detected by western blot assay.
RESULTS: The expression of CASC20 was increased in GC tumor tissues and various GC cell lines. High CASC20 expression was correlated with a high risk of lymphatic metastasis and poor prognosis in GC patients. In vitro assays showed that silencing CASC20 reduced cell proliferation, migration, and invasion in GC cells. Mechanistic studies revealed that CASC20 exhibits oncogenic functions by regulating MEMO1 expression through competitive endogenous binding to miR-143-5p, leading to induction of epithelial-mesenchymal transition.
CONCLUSIONS: Our findings indicate that CASC20 serves as a tumor promoter by regulating metastasis in GC via the miR-143-5p/MEMO1 axis. CASC20 may be a potential therapeutic target for GC.
摘要：
背景：胃癌（GC）被认为是最广泛的恶性肿瘤之一。新的证据表明，lncRNAs在GC进展过程中可以作为重要的癌基因或肿瘤抑制因子发挥作用。
目的：探讨lncRNA癌易感性20(CASC20)在GC细胞增殖和转移中的作用及其机制。
方法：使用数据挖掘和临床样本评估CASC20在GC和癌旁组织中的表达。CASC20在GC细胞中通过短干扰RNA下调。通过CCK-8测定评估细胞增殖,通过伤口愈合和Transwell测定检测细胞迁移和侵袭。Westernblot法检测上皮间质转化相关蛋白的表达。
结果：CASC20在GC肿瘤组织和各种GC细胞系中的表达增加。CASC20高表达与GC患者淋巴转移的高风险和不良预后相关。体外实验表明沉默CASC20可降低细胞增殖,迁移,和侵袭GC细胞。机制研究表明，CASC20通过竞争性内源性结合miR-143-5p来调节MEMO1表达，从而表现出致癌功能。导致上皮-间质转化的诱导。
结论：我们的发现表明，CASC20通过miR-143-5p/MEMO1轴调节GC中的转移而充当肿瘤启动子。CASC20可能是GC的潜在治疗靶点。
目的：探讨lncRNA癌易感性20(CASC20)在GC细胞增殖和转移中的作用及其机制。
方法：使用数据挖掘和临床样本评估CASC20在GC和癌旁组织中的表达。CASC20在GC细胞中通过短干扰RNA下调。通过CCK-8测定评估细胞增殖,通过伤口愈合和Transwell测定检测细胞迁移和侵袭。Westernblot法检测上皮间质转化相关蛋白的表达。
结果：CASC20在GC肿瘤组织和各种GC细胞系中的表达增加。CASC20高表达与GC患者淋巴转移的高风险和不良预后相关。体外实验表明沉默CASC20可降低细胞增殖,迁移,和侵袭GC细胞。机制研究表明，CASC20通过竞争性内源性结合miR-143-5p来调节MEMO1表达，从而表现出致癌功能。导致上皮-间质转化的诱导。
结论：我们的发现表明，CASC20通过miR-143-5p/MEMO1轴调节GC中的转移而充当肿瘤启动子。CASC20可能是GC的潜在治疗靶点。
