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Linc00662/miR-16-5p/FASN在宫颈癌中的预后价值及对肿瘤进展的调控

Prognostic value of Linc00662/miR-16-5p/FASN in cervical cancer and regulation of tumor progression.

作者信息

Yang Yu, Guo Zhanping

机构信息

Department of East District Laboratory, Xinxiang Central Hospital, Northwest corner of the intersection of East Rongxiao Road and Dongming Avenue, Muye District, Xinxiang City, Henan Province, 453001, China.

出版信息

Hereditas. 2025 Aug 5;162(1):151. doi: 10.1186/s41065-025-00520-6.

DOI:10.1186/s41065-025-00520-6
PMID:40764609
Abstract

BACKGROUND

Cervical cancer (CC) is the world's single most frequent gynecological cancer, is more than 500,000 new annual cases globally, and is a serious threat to women's reproductive health. LncRNAs have significant effects on human diseases; nevertheless, the expression of Linc00662 in CC and its mechanism of action are not yet entirely clear. The goal of the work was to investigate the expression, prognostic value and biological utility of Linc00662 in CC progression and to identify its underlying mechanisms in molecular terms.

METHODS

Expression levels of Linc00662, miR-16-5p and FASN in CC tissues and cells were detected through real-time quantitative PCR. Determination of cell proliferative capacity by CCK-8. Cell migration and invasion were assessed through Transwell assay. Binding of Linc00662 to miR-16-5p was mediated through a dual-luciferase reporter gene test was validated.

RESULTS

Linc00662 expression levels were significantly elevated in CC. High Linc00662 expression was strongly linked to increased tumor size, later FIGO staging, poorer tumor differentiation, mesenchymal infiltration, and lymph node metastasis, and high Linc00662 expression predicted a poor prognosis. Silencing Linc00662 reduced the proliferation, migration, and invasion of CC cells. Furthermore, Linc00662 negatively regulated miR-16-5p and indirectly regulated the upregulation of FASN expression.

CONCLUSIONS

Linc00662 positively regulates FASN expression through targeting miR-16-5p and facilitates CC cell proliferation, migration and invasion, promoting CC progression.

摘要

背景

宫颈癌(CC)是全球最常见的妇科癌症,全球每年新增病例超过50万,严重威胁女性生殖健康。长链非编码RNA(lncRNAs)对人类疾病有显著影响;然而,Linc00662在宫颈癌中的表达及其作用机制尚不完全清楚。本研究旨在探讨Linc00662在宫颈癌进展中的表达、预后价值和生物学功能,并从分子层面确定其潜在机制。

方法

通过实时定量PCR检测宫颈癌组织和细胞中Linc00662、miR-16-5p和脂肪酸合酶(FASN)的表达水平。采用CCK-8法测定细胞增殖能力。通过Transwell实验评估细胞迁移和侵袭能力。通过双荧光素酶报告基因实验验证Linc00662与miR-16-5p的结合。

结果

Linc00662在宫颈癌中的表达水平显著升高。Linc00662高表达与肿瘤体积增大、国际妇产科联盟(FIGO)分期较晚、肿瘤分化较差、间质浸润和淋巴结转移密切相关,且Linc00662高表达预示预后不良。沉默Linc00662可降低宫颈癌细胞的增殖、迁移和侵袭能力。此外,Linc00662负向调节miR-16-5p,并间接调节FASN表达上调。

结论

Linc00662通过靶向miR-16-5p正向调节FASN表达,促进宫颈癌细胞增殖、迁移和侵袭,推动宫颈癌进展。

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