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长链非编码RNA BCRT1缺失通过海绵吸附miR-432-5p/CCR7轴抑制宫颈癌细胞生长。

LncRNA BCRT1 depletion suppresses cervical cancer cell growth via sponging miR-432-5p/CCR7 axis.

作者信息

Wang Xiaoli, Li Huifang, Li Naihua, Yang Hailan, Bai Xiangdong

机构信息

Department of Gynaecology, Shanxi Integrated Traditional Chinese and Western Medicine Hospital, Shanxi Medical University, No. 85, Jiefang South Road, Taiyuan, 030001 Shanxi China.

Department of Gynaecology, Shanxi Medical University, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi China.

出版信息

3 Biotech. 2024 Jan;14(1):17. doi: 10.1007/s13205-023-03863-x. Epub 2023 Dec 19.

Abstract

UNLABELLED

Breast cancer-related transcript 1 (BCRT1), a lncRNA that is overexpressed in several human cancers, facilitates the progression of breast cancer and osteosarcoma. Nevertheless, the function of BCRT1 in cervical cancer (CC) still remains unknown. In this study, BCRT1 was significantly overexpressed in CC tissues and correlated with the advanced stage of CC patients. BCRT1 depletion dampened CC cell proliferation, and drives cell apoptosis and cell cycle inhibition. Mechanistically, BCRT1 bound miR-432-5p and negatively modulated miR-432-5p's expression in CC cells. Reduced miR-452-3p expression was observed in CC tissues and exerted tumor suppressive function in CC cell growth. Further mechanism study revealed that CCR7 was clarified as a target of miR-432-5p and was inhibited following BCRT1 depletion. CCR7 transfection could recover CC cell growth that was suppressed with BCRT1 down-regulation. These results revealed the novel function of BCRT1/miR-432-5p/CCR7 pathway in CC, suggesting BCRT1 might be a potential biomarker and target for CC treatment.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s13205-023-03863-x.

摘要

未标记

乳腺癌相关转录本1(BCRT1)是一种在多种人类癌症中过表达的长链非编码RNA,可促进乳腺癌和骨肉瘤的进展。然而,BCRT1在宫颈癌(CC)中的功能仍不清楚。在本研究中,BCRT1在CC组织中显著过表达,且与CC患者的晚期阶段相关。BCRT1的缺失抑制了CC细胞增殖,并驱动细胞凋亡和细胞周期抑制。机制上,BCRT1与miR-432-5p结合并负向调节CC细胞中miR-432-5p的表达。在CC组织中观察到miR-452-3p表达降低,且其在CC细胞生长中发挥肿瘤抑制功能。进一步的机制研究表明,CCR7被确认为miR-432-5p的靶点,并且在BCRT1缺失后受到抑制。CCR7转染可恢复因BCRT1下调而受到抑制的CC细胞生长。这些结果揭示了BCRT1/miR-432-5p/CCR7通路在CC中的新功能,表明BCRT1可能是CC治疗的潜在生物标志物和靶点。

补充信息

在线版本包含可在10.1007/s13205-023-03863-x获取的补充材料。

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