ELFN1-AS1 accelerates cell proliferation, invasion and migration via regulating miR-497-3p/CLDN4 axis in ovarian cancer.
ELFN1-AS1 accelerates cell proliferation, invasion and migration via regulating miR-497-3p/CLDN4 axis in ovarian cancer.
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DOI：
10.1080/21655979.2020.1797281
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发表时间：
2020-12
期刊：
影响因子：
4.9
通讯作者：
Fu Y
中科院分区：
文献类型：
--
作者：
Jie Y;Ye L;Chen H;Yu X;Cai L;He W;Fu Y
先前的研究表明，长非编码RNA（LncRNA）参与包括卵巢癌（OV）在内的多种癌症的进展。 LncRNA ELFN1-AS1 在许多癌症中充当癌基因，但其在 OV 中的潜在作用尚不清楚。在本研究中，我们旨在阐明ELFN1-AS1在OV中的生物学作用和分子机制。我们发现 ELFN1-AS1 在 OV 组织和细胞系中显着上调。 ELFN1-AS1的高表达与OV患者的不良预后相关。 ELFN1-AS1 的敲低抑制了 SKOV3 细胞系的增殖、迁移和侵袭，并抑制了异种移植卵巢模型中的肿瘤生长。从机制上讲，ELFN1-AS1通过海绵miR-497-3p促进SKOV3细胞的增殖、迁移和侵袭。此外，CLDN4 被证实是 miR-497-3p 的靶标。拯救实验表明，抑制 miR-497-3p 可以部分逆转 ELFN1-AS1 沉默对 SKOV3 细胞系增殖、迁移和侵袭的抑制作用。综上所述，我们的研究结果表明，ELFN1-AS1 通过直接与 miR-497-3p 相互作用来调节 CLDN4 的表达，从而在卵巢癌中发挥癌基因的作用。结果表明 ELFN1-AS1 可能作为 OV 的一个有前途的治疗靶点。
Previous studies indicated that long non-coding RNAs (LncRNAs) were involved in the progression of multiple cancers including ovarian cancer (OV). LncRNA ELFN1-AS1 functioned as an oncogene in many cancers, but its potential roles in OV were largely unclear. In the current study, we were aimed at clarifying the biological roles and molecular mechanisms of ELFN1-AS1 in OV. We found that ELFN1-AS1 was significantly upregulated in OV tissues and cell lines. High expression of ELFN1-AS1 was associated with poor prognosis in OV patients. Knockdown of ELFN1-AS1 inhibited the proliferation, migration and invasion of SKOV3 cell lines and repressed tumor growth in xenografted ovarian models. Mechanistically, ELFN1-AS1 promoted the proliferation, migration and invasion of SKOV3 cells by sponging miR-497-3p. Additionally, CLDN4 was verified to be the target of miR-497-3p. Rescue experiments revealed that miR-497-3p inhibition could partly reverse the inhibitory effect of ELFN1-AS1 silencing on proliferation, migration and invasion of SKOV3 cell lines. Taken together, our findings indicated that ELFN1-AS1 acted as an oncogene in ovarian cancer through regulating the expression of CLDN4 by directly interacting with miR-497-3p. The results suggested that ELFN1-AS1 might act as a promising therapeutic target for OV.
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影响因子：
4.8
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
10.3322/caac.20113
发表时间：
2011-05
期刊：
CA: a cancer journal for clinicians
影响因子：
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作者：
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通讯作者：
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影响因子：
4
作者：
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