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长链非编码RNA HMMR-AS1通过调控miR-627-3p/PTN轴促进卵巢癌细胞的恶性进展。

The lncrna HMMR-AS1 promotes the malignant progression of ovarian cancer cells by regulating the miR-627-3p/PTN axis.

作者信息

He Jiaren, Tian Fei, Li Jie, Zhang Yunxia, Chu Zhaoping

机构信息

HeBei General Hospital, Shijiazhuang, Hebei Province, 050051, China.

North China University of Science and Technology, Tangshan, Hebei Province, 063210, China.

出版信息

J Ovarian Res. 2025 Jun 3;18(1):119. doi: 10.1186/s13048-025-01691-6.

Abstract

BACKGROUND

LncRNAs are crucial regulators of ovarian cancer, playing a significant role in malignant transformation and closely linked to poor prognosis. Therefore, it is crucial to investigate the impact of lncRNAs on the malignant biological behavior of ovarian cancer and to understand their underlying molecular mechanisms.

METHODS

Gene expression levels were measured using qRT-PCR. The malignant biological behavior of cells was assessed through cell biological function assays. The binding sites of target genes were predicted through bioinformatics analysis, and gene targeting relationships were verified using a dual-luciferase reporter gene(DLRG) assay. Protein expression levels were analyzed using Western blotting.

RESULTS

In ovarian cancer cells, the expression levels of HMMR-AS1 and PTN were upregulated, whereas the expression of miR-627-3p was downregulated. Cell biological function experiments demonstrated that HMMR-AS1 and PTN could enhance the malignant behavior of ovarian cancer cells, while miR-627-3p exhibited the opposite effect. The DLRG assay indicated that lncRNA HMMR-AS1 directly targets miR-627-3p, with PTN identified as the target gene of miR-627-3p. Western blotting indicated that lncRNA HMMR-AS1 promoted the expression of PTN protein, while miR-627-3p inhibited it. Furthermore, it was demonstrated that miR-627-3p or PTN could partially reverse the effects of lncRNA HMMR-AS1 on the malignant phenotype of ovarian cancer cells.

CONCLUSION

In summary, HMMR-AS1 is highly expressed in ovarian cancer and plays a carcinogenic role by regulating the miR-627-3p/PTN axis and suggest that targeting HMMR-AS1 is a potential strategy for ovarian cancer treatment.

摘要

背景

长链非编码RNA(lncRNAs)是卵巢癌的关键调节因子,在恶性转化中起重要作用,且与预后不良密切相关。因此,研究lncRNAs对卵巢癌恶性生物学行为的影响并了解其潜在分子机制至关重要。

方法

采用qRT-PCR检测基因表达水平。通过细胞生物学功能试验评估细胞的恶性生物学行为。通过生物信息学分析预测靶基因的结合位点,并使用双荧光素酶报告基因(DLRG)试验验证基因靶向关系。采用蛋白质免疫印迹法分析蛋白质表达水平。

结果

在卵巢癌细胞中,HMMR-AS1和PTN的表达水平上调,而miR-627-3p的表达下调。细胞生物学功能实验表明,HMMR-AS1和PTN可增强卵巢癌细胞的恶性行为,而miR-627-3p则表现出相反的作用。DLRG试验表明lncRNA HMMR-AS1直接靶向miR-627-3p,PTN被确定为miR-627-3p的靶基因。蛋白质免疫印迹法表明lncRNA HMMR-AS1促进PTN蛋白的表达,而miR-627-3p则抑制其表达。此外,还证明miR-627-3p或PTN可部分逆转lncRNA HMMR-AS1对卵巢癌细胞恶性表型的影响。

结论

综上所述,HMMR-AS1在卵巢癌中高表达,通过调节miR-627-3p/PTN轴发挥致癌作用,提示靶向HMMR-AS1是卵巢癌治疗的潜在策略。

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