Abstract：
Background: Long noncoding RNAs (lncRNAs) contribute to the initiation and progression of gastric cancer (GC). The purpose of this study is to examine the potential role of lncRNA colorectal neoplasia differentially expressed (CRNDE) in modulating the expression of migration and invasion enhancer 1 (MIEN1) through the suppression of miR-136-5p in GC. Methods: The biological roles of CRNDE, miR-136-5p, and MIEN1 in GC were assessed both in laboratory settings and through the examination of clinical samples. Results: CRNDE was found to be significantly increased in GC tissues, and this upregulation was associated with an unfavorable prognosis of GC patients. In vitro experiments showed that inhibiting cell growth and migration, along with promoting apoptosis in GC cells, could be achieved by either disabling CRNDE or MIEN1, or by increasing the expression of miR-136-5p. MIEN1 is a specific recipient of miR-136-5p, and the anticancer effects of miR-136-5p can be counteracted by the increased expression of MIEN1. Through the examination of clinical specimens, it has been observed that there is a significant positive correlation between the expression of MIEN1 and CRNDE. In contrast, miR-136-5p expression in GC tissues shows a negative correlation. Conclusion: A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.
摘要：
背景：长链非编码RNA（lncRNA）有助于胃癌（GC）的发生和发展。这项研究的目的是研究lncRNA结直肠肿瘤差异表达（CRNDE）在通过抑制GC中的miR-136-5p调节迁移和侵袭增强子1（MIEN1）表达中的潜在作用。方法：CRNDE的生物学作用，miR-136-5p,在实验室环境中和通过临床样本检查评估GC中的MIEN1。结果：发现GC组织中CRNDE明显增加，这种上调与GC患者的预后不良有关。体外实验表明,抑制细胞生长和迁移,在促进GC细胞凋亡的同时，可以通过禁用CRNDE或MIEN1，或通过增加miR-136-5p的表达来实现。MIEN1是miR-136-5p的特定受体，miR-136-5p的抗癌作用可以通过增加MIEN1的表达来抵消。通过对临床标本的检查,已经观察到MIEN1的表达与CRNDE之间存在显着正相关。相比之下,miR-136-5p在GC组织中的表达呈负相干。结论：先前未探索的GC治疗靶标涉及CRNDE/miR-136-5p/MIEN1信号转导级联。
