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长链非编码RNA ABHD11-AS1通过吸附miR-876-5p上调钙调蛋白2以促进甲状腺癌转移。

LncRNA ABHD11-AS1 Elevates CALM2 to Promote Metastasis of Thyroid Cancer Through Sponging miR-876-5p.

作者信息

Lv Juan, Chen Fukun, Lv Ling, Zhang Lu, Zou Huangren, Liu Yanlin, Bai Yuke, Fang Ruotong, Qin Tiantian, Deng Zhiyong

机构信息

Department of Nuclear Medicine, Yunnan Cancer Hospital, the Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, 650118, Yunnan Province, China.

出版信息

Biochem Genet. 2025 Mar 21. doi: 10.1007/s10528-025-11072-9.

Abstract

In the past decade, the treatment of thyroid cancer (TC) has been brought to a new era, but tumor metastasis still is an intractable difficulty in clinical. LncRNA ABHD11-AS1 has been confirmed to be involved in TC progression. However, its specific mechanism remains unknown. Tissues from TC patients and TC cells served as mainly experimental subjects in this study. The migration of TC cells was assessed using the scratch assay, and the ability of cell invasion was evaluated by transwell assay. RT-qPCR and western blot were conducted to determine the levels of related genes and proteins. The dual-luciferase reporter assay was used to validate the relationships among ABHD11-AS1, miR-876-5p and CALM2. ABHD11-AS1 and CALM2 are elevated in TC cancer samples and cells, while the expression of miR-876-5p is reduced. Subsequently, the ability of TC cells to migrate, invade and EMT was inhibited by both ABHD11-AS1 knockdown or miR-876-5p overexpression. Moreover, the suppression of malignant characteristics in TC cells resulting from ABHD11-AS knockdown was counteracted by the inhibition of miR-876-5p or the upregulation of CALM2. On the mechanism, ABHD11-AS1 elevated CALM2 and promoted the malignant development of TC cells by acting as a miR-876-5p sponge. ABHD11-AS1 mediated the miR-876-5p/CALM2 axis to drive the metastasis of thyroid cancer.

摘要

在过去十年中,甲状腺癌(TC)的治疗进入了一个新时代,但肿瘤转移在临床上仍然是一个棘手的难题。长链非编码RNA ABHD11-AS1已被证实参与甲状腺癌进展。然而,其具体机制仍不清楚。本研究以甲状腺癌患者组织和甲状腺癌细胞作为主要实验对象。采用划痕实验评估甲状腺癌细胞的迁移能力,通过Transwell实验评估细胞侵袭能力。进行RT-qPCR和蛋白质免疫印迹以测定相关基因和蛋白质的水平。采用双荧光素酶报告基因实验验证ABHD11-AS1、miR-876-5p和CALM2之间的关系。ABHD11-AS1和CALM2在甲状腺癌样本和细胞中表达升高,而miR-876-5p的表达降低。随后,敲低ABHD11-AS1或过表达miR-876-5p均可抑制甲状腺癌细胞的迁移、侵袭和上皮-间质转化能力。此外,抑制miR-876-5p或上调CALM2可抵消敲低ABHD11-AS1对甲状腺癌细胞恶性特征的抑制作用。机制上,ABHD11-AS1作为miR-876-5p的海绵,上调CALM2并促进甲状腺癌细胞的恶性发展。ABHD11-AS1通过介导miR-876-5p/CALM2轴驱动甲状腺癌转移。

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