miR-214 inhibits invasion and migration via downregulating GALNT7 in esophageal squamous cell cancer
miR-214 inhibits invasion and migration via downregulating GALNT7 in esophageal squamous cell cancer
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miR-214通过下调GALNT7抑制食管鳞状细胞癌的侵袭和迁移
DOI：
10.1007/s13277-016-5320-7
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发表时间：
2016-11-01
期刊：
影响因子：
--
通讯作者：
Chen, Hezhong
中科院分区：
文献类型：
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作者：
Lu, Qijue;Xu, Li;Chen, Hezhong
已有研究证实miR-214在多种肿瘤的侵袭和迁移中具有重要意义。已经证明UDP-N-乙酰基-α-D-半乳糖胺：多肽N-乙酰基半乳糖胺转移酶7（GALNT 7）是miR-214的推定靶标。本研究旨在探讨miR-214和GALNT 7在食管鳞状细胞癌（ESCC）侵袭和迁移中的作用。与相应的非肿瘤组织相比，miR-214在肿瘤中的表达显著下调，而GALNT 7显示出相反的趋势。miR-214的低表达和GALNT 7的高表达与食管鳞癌的分化程度（P = 0.004）、浸润深度（P = 0.013）和淋巴结转移（P = 0.012）呈正相关。功能研究表明，过表达miR-214或敲低GALNT 7可减弱Eca 109、TE 1和KYSE 150的侵袭和迁移能力。此外，致瘤性分析显示，注射含有miR-214模拟物或GALNT 7小干扰RNA的细胞的我们小鼠形成的肿瘤比miR-214抑制剂组明显更小。因此，我们得出结论，miR-214显示出成为ESCC诊断标志物和治疗靶点的潜力。
Previous studies verified that miR-214 is of great significance in the invasion and migration of a variety of cancers. It has been demonstrated that UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyltransferase 7(GALNT7) is a putative target of miR-214. We performed this study to figure out howmiR-214 and GALNT7 play their roles in the invasion and migration of esophageal squamous cell carcinoma(ESCC). The expression of miR-214 was significantly downregulated in tumors compared to the corresponding non-tumor tissues while GALNT7 showed an opposite tendency. The low expression of miR-214 and the high expression of GALNT7 were found positively correlated with poor tumor differentiation (P = 0.004), tumor invasion (P = 0.013), and lymph nodemetastasis (P = 0.012) in ESCC patients. Functional study demonstrated that overexpression of miR-214 or knockdown of GALNT7 could weaken invasive and migratory ability in Eca109, TE1, and KYSE150. Moreover, tumorigenicity assay showed us mice injected with cells containing miR-214 mimic or GALNT7 small interfering RNA formed substantially smaller tumors than that in miR-214 inhibitor group. Consequently, we concluded that miR-214 shows potential to be a diagnostic marker and therapeutic target in ESCC.