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Depressing hsa_circ_0058092 functions an integrated anti-proliferation and anti-motility role in gastric cancer partially through targeting miR-1294/SIX1 axis
Applied Biological Chemistry ( IF 2.3 ) Pub Date : 2022-07-08 , DOI: 10.1186/s13765-022-00715-9
Jianming Fang , Jianxin Huang , Xiaodong Zhang

Fibronectin 1-derived circular RNA hsa_circ_0058092 is a novel potential oncogene in gastric cancer (GC). Yet, previous studies have not determined the role of hsa_circ_0058092 GC progression and the underlying mechanism. Herein, we investigated its role and competing endogenous RNA (ceRNA) pathway in the development of GC. The results showed that hsa_circ_0058092 was substantially upregulated in GC patients’ tissues and cells, allied with upregulated SIX1 and downregulated miR-1294 compared with normal gastric tissues and cells. There were linear correlations among hsa_circ_0058092, miR-1294 and SIX1 levels in GC tumors. Moreover, hsa_circ_0058092 acted as a miR-1294 sponge, and miR-1294 targeted SIX1. Functionally, colony formation, EdU positive rate, tumor growth of GC cells, as well as ki-67 expression in xenograft tumors was greatly suppressed by depressing hsa_circ_0058092. Besides, hsa_circ_0058092 knockdown repressed GC cell migration and invasion, accompanied with increased E-cadherin expression and descended N-cadherin expression. Moreover, inhibiting miR-1294 expression could counteract hsa_circ_0058092 knockdown-mediated effects in GC cells. The inhibitory effects of miR-1294 mimics on GC cell malignancy were relieved by increasing SIX1 expression. Further, hsa_circ_0058092 depletion repressed SIX1 protein expression by interacting with miR-1294. Hsa_circ_0058092 was oncogenic in GC cell proliferation and motility via ceRNA pathway of hsa_circ_0058092/miR-1294/SIX1.

中文翻译:

部分通过靶向 miR-1294/SIX1 轴抑制 hsa_circ_0058092 在胃癌中发挥综合的抗增殖和抗运动作用

纤连蛋白 1 衍生的环状 RNA hsa_circ_0058092 是胃癌 (GC) 中一种新的潜在癌基因。然而,先前的研究尚未确定 hsa_circ_0058092 GC 进展的作用及其潜在机制。在这里,我们研究了它在 GC 发展中的作用和竞争性内源性 RNA (ceRNA) 途径。结果表明,与正常胃组织和细胞相比,hsa_circ_0058092 在 GC 患者的组织和细胞中显着上调,与上调的 SIX1 和下调的 miR-1294 相关。GC肿瘤中hsa_circ_0058092、miR-1294和SIX1水平之间存在线性相关。此外,hsa_circ_0058092 充当 miR-1294 海绵,miR-1294 靶向 SIX1。功能上,集落形成,EdU 阳性率,GC 细胞的肿瘤生长,通过抑制 hsa_circ_0058092 极大地抑制了异种移植肿瘤中的 ki-67 表达。此外,hsa_circ_0058092 敲低抑制了 GC 细胞迁移和侵袭,伴随着 E-cadherin 表达增加和 N-cadherin 表达下降。此外,抑制 miR-1294 表达可以抵消 GC 细胞中 hsa_circ_0058092 敲低介导的作用。通过增加 SIX1 的表达,miR-1294 模拟物对 GC 细胞恶性肿瘤的抑制作用得到缓解。此外,hsa_circ_0058092 消耗通过与 miR-1294 相互作用抑制了 SIX1 蛋白的表达。Hsa_circ_0058092 通过 hsa_circ_0058092/miR-1294/SIX1 的 ceRNA 途径在 GC 细胞增殖和运动中致癌。伴随着 E-cadherin 表达增加和 N-cadherin 表达下降。此外,抑制 miR-1294 表达可以抵消 GC 细胞中 hsa_circ_0058092 敲低介导的作用。通过增加 SIX1 的表达,miR-1294 模拟物对 GC 细胞恶性肿瘤的抑制作用得到缓解。此外,hsa_circ_0058092 消耗通过与 miR-1294 相互作用抑制了 SIX1 蛋白的表达。Hsa_circ_0058092 通过 hsa_circ_0058092/miR-1294/SIX1 的 ceRNA 途径在 GC 细胞增殖和运动中致癌。伴随着 E-cadherin 表达增加和 N-cadherin 表达下降。此外,抑制 miR-1294 表达可以抵消 GC 细胞中 hsa_circ_0058092 敲低介导的作用。通过增加 SIX1 的表达,miR-1294 模拟物对 GC 细胞恶性肿瘤的抑制作用得到缓解。此外,hsa_circ_0058092 消耗通过与 miR-1294 相互作用抑制了 SIX1 蛋白的表达。Hsa_circ_0058092 通过 hsa_circ_0058092/miR-1294/SIX1 的 ceRNA 途径在 GC 细胞增殖和运动中致癌。hsa_circ_0058092 缺失通过与 miR-1294 相互作用抑制了 SIX1 蛋白的表达。Hsa_circ_0058092 通过 hsa_circ_0058092/miR-1294/SIX1 的 ceRNA 途径在 GC 细胞增殖和运动中致癌。hsa_circ_0058092 缺失通过与 miR-1294 相互作用抑制了 SIX1 蛋白的表达。Hsa_circ_0058092 通过 hsa_circ_0058092/miR-1294/SIX1 的 ceRNA 途径在 GC 细胞增殖和运动中致癌。
更新日期:2022-07-10
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