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长链非编码 RNA DUXAP8 通过 miR-223-3p 介导的 CXCR4 调节促进甲状腺乳头状癌细胞的增殖、迁移和侵袭。

Long non-coding RNA DUXAP8 promotes the cell proliferation, migration, and invasion of papillary thyroid carcinoma via miR-223-3p mediated regulation of CXCR4.

机构信息

Department of Ultrasound, China-Japan Union Hospital of Jilin University , Changchun, People's Republic of China.

出版信息

Bioengineered. 2021 Dec;12(1):496-506. doi: 10.1080/21655979.2021.1882134.

Abstract

Papillary thyroid carcinoma (PTC) is a differentiated type of thyroid malignancy with a high incidence. Long non-coding RNA (lncRNA) DUXAP8 has been reported to participate in the proliferation, migration, and invasion of several cancer types. However, its association with PTC has not yet been reported. The current study aimed to investigate the role of DUXAP8 in PTC and revealed the underlying mechanisms. The expression of DUXAP8 was knocked down in two PTC cell lines and the effects of DUXAP8 on the PTC biological behavior were examined by cell counting kit-8 (CCK-8), wound healing, and transwell invasion assays. Luciferase reporter assay was used to detect the binding activity between miR-223-3p and DUXAP8. We found that knockdown of DUXAP8 inhibited the proliferation, migration, and invasion of PTC cells. DUXAP8 could sponge miR-223-3p through the specific binding site. CXCR4 was a target of miR-223-3p. The malignant phenotypes of the PTC cells were suppressed by the over-expression of miR-223-3p. Moreover, miR-223-3p inhibition or CXCR4 over-expression partly restored the proliferation, migration, and invasion activities of DUXAP8-downregulated PTC cells. The results evidenced that DUXAP8 acted as an oncogene in PTC, these effects seemed to partly dependent on the miR-223-3p/CXCR4 axis.

摘要

甲状腺乳头状癌(PTC)是一种分化型甲状腺恶性肿瘤,发病率较高。长链非编码 RNA(lncRNA)DUXAP8 已被报道参与多种癌症类型的增殖、迁移和侵袭。然而,其与 PTC 的关联尚未报道。本研究旨在探讨 DUXAP8 在 PTC 中的作用及其潜在机制。在两种 PTC 细胞系中敲低 DUXAP8 的表达,通过细胞计数试剂盒-8(CCK-8)、划痕愈合和 Transwell 侵袭实验检测 DUXAP8 对 PTC 生物学行为的影响。荧光素酶报告实验用于检测 miR-223-3p 和 DUXAP8 之间的结合活性。结果发现,敲低 DUXAP8 抑制了 PTC 细胞的增殖、迁移和侵袭。DUXAP8 通过特定的结合位点吸附 miR-223-3p。CXCR4 是 miR-223-3p 的靶基因。过表达 miR-223-3p 抑制了 PTC 细胞的恶性表型。此外,miR-223-3p 抑制或 CXCR4 过表达部分恢复了 DUXAP8 下调的 PTC 细胞的增殖、迁移和侵袭活性。结果表明,DUXAP8 在 PTC 中发挥癌基因作用,这些作用似乎部分依赖于 miR-223-3p/CXCR4 轴。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6dd/8291844/63a2c7ed4e29/KBIE_A_1882134_UF0001_OC.jpg

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