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ILF3-AS1 通过与 miR-4429 结合来上调 RAB14,从而促进乳腺癌细胞增殖和抑制细胞凋亡。

ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14.

机构信息

Department of Medical Imaging, 26488Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, China.

Department of Breast Surgery, 26488Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, China.

出版信息

Hum Exp Toxicol. 2021 Jul;40(7):1183-1193. doi: 10.1177/0960327121989422. Epub 2021 Feb 2.

Abstract

As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.

摘要

作为女性癌症相关死亡的主要原因之一,乳腺癌自 20 世纪 70 年代以来在全球的发病率增加了 30%。最近,越来越多的研究表明,长非编码 RNA ILF3-AS1 参与了多种癌症的进展。然而,ILF3-AS1 在乳腺癌中的作用在很大程度上仍然未知。在本研究中,我们发现 ILF3-AS1 在乳腺癌组织和细胞中高表达。ILF3-AS1 沉默抑制乳腺癌细胞增殖、迁移和侵袭,并促进细胞凋亡。ILF3-AS1 在乳腺癌细胞中与 miR-4429 结合。此外,RAB14 是 miR-4429 的下游靶标,miR-4429 的表达与乳腺癌组织中 RAB14 或 ILF3-AS1 的表达呈负相关。挽救实验的结果表明,RAB14 的过表达可以逆转 ILF3-AS1 敲低对乳腺癌细胞增殖、迁移和侵袭的抑制作用。总的来说,ILF3-AS1 通过与 miR-4429 相互作用来调节 RAB14,从而促进乳腺癌细胞的恶性表型,这可能为乳腺癌的潜在机制提供新的见解。

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