Long Non-Coding RNA LEF1-AS1 Promotes Migration, Invasion and Metastasis of Colon Cancer Cells Through miR-30-5p/SOX9 Axis (Retracted Article)
Long Non-Coding RNA LEF1-AS1 Promotes Migration, Invasion and Metastasis of Colon Cancer Cells Through miR-30-5p/SOX9 Axis (Retracted Article)
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DOI：
10.2147/ott.s232839
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发表时间：
2020-01-01
影响因子：
4
通讯作者：
Wang, Yongpeng
中科院分区：
文献类型：
--
作者：
Sun, Ting;Liu, Zhexian;Wang, Yongpeng
前言：长链非编码RNA（lncRNA）的异常表达与结肠癌的发生和发展有关。类磷脂增强子结合因子1反义RNA（LEF 1-AS 1）是一种高度保守的新发现的长链非编码RNA，在结肠癌中表达上调并与预后不良相关，但其确切作用尚不清楚。本研究通过细胞存活率测定、集落形成测定、细胞凋亡测定、细胞凋亡测定等方法，分析LEF 1-AS 1在结肠癌中的生物学功能，结果：LEF 1-AS 1在结肠癌患者中表达上调，与患者的总生存率和无复发生存率相关。此外，LEF 1-AS 1在HT 29和T84细胞中的高表达促进了细胞的迁移、侵袭、非贴壁依赖性生长、异种移植瘤形成和肺转移，而在COLO 320细胞中的低表达抑制了细胞的迁移、侵袭、非贴壁依赖性生长和异种移植瘤形成。此外，LEF 1-AS 1与结肠癌中的miR-30- 5 p直接相互作用并呈负相关，而SOX 9是miR-30- 5 p的下游靶点。结论：LEF 1-AS 1基因的过表达可促进结肠癌细胞的迁移、侵袭、非贴壁依赖性生长和移植瘤形成，其作用机制可能部分通过miR-30- 5 p/SOX 9轴。致癌基因LEF 1-AS 1可能是结肠癌的一个潜在的预后生物标志物。
Introduction: Aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in the tumorigenesis and progression of colon cancer. Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long noncoding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.Materials and Methods: In our study, the biological functions of LEF1-AS1 in colon cancer were analyzed by cell viability assay, colony formation assay, scratch wound healing assay, transwell cell invasion assay, soft agar assay, luciferase reporter assay, pull down assay, tumor xenograft model and Western blot.Results: We found that LEF1-AS1 was upregulated in colon cancer patients and correlated with poor overall survival and recurrent-free survival. Besides, enforced expression of LEF1-AS1 in HT29 and T84 cells promoted migration, invasion, anchorage-independent growth, tumor xenograft formation and lung metastasis, while knockdown of LEF1-AS1 in COLO320 cells suppressed cell migration, invasion, anchorage-independent growth and tumor xenograft formation. In addition, LEF1-AS1 was directly interacted and inversely correlated with miR-30-5p in colon cancer, and SOX9 was a downstream target for miR-30-5p. LEF1-AS1 overexpression increased the expression level of SOX9, and restoration of SOX9 attenuated the effects caused by LEF1-AS1 knockdown in cell migration, invasion, anchorage-independent growth and tumor xenograft formation.Conclusion: Our results indicated that LEF1-AS1 promotedmigration, invasion and metastasis of colon cancer cells partially through miR-30-5p/SOX9 axis. The oncogenic LEF1-AS1 could be a potential prognostic biomarker for colon cancer.