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miR-98-3p/VEGFA轴在卵巢瘤中调解MALAT1诱导的血管生成

Mengxin Zhang¹, Yu Zhang¹, Jiabao Xu¹

¹Department of Immunology and Microbiology, Basic Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.

Experimental cell research

|December 4, 2025

概括

这项研究揭示了一条涉及MALAT1,microRNA 98-3p (miR-98-3p) 和VEGFA的新途径,它影响卵巢癌的生长和血管形成. 针对这一轴可能为卵巢癌提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

微RNA miR-98-3p在卵巢癌中的作用尚不清楚.
驱动卵巢癌血管生成的分子机制需要进一步阐明.

研究的目的:

在卵巢癌中识别和描述涉及MALAT1,miR-98-3p和VEGFA的调节轴.
研究这一轴对卵巢癌扩散,迁移和血管生成的功能影响.

主要方法:

在MALAT1在HEY-T30细胞中被淘汰后,进行了RNA测序.
用路西法酶记者测定来确认MALAT1,miR-98-3p和VEGFA之间的直接相互作用.
在体外 (HUVEC管形成,增殖,迁移) 和体内 (异种移植模型) 进行了功能测试.

主要成果:

MALAT1 作为 miR-98-3p 的竞争性内源RNA,而 VEGFA 是 miR-98-3p 的直接目标.
提高MALAT1和VEGFA表达与卵巢癌患者的生存率差相关.
在体内,MALAT1倒置或miR-98-3p过度表达抑制了HUVEC管形成,增殖,迁移,并减少了瘤生长,血管化和VEGFA/MMP表达.

结论:

一个新的MALAT1/miR-98-3p/VEGFA调节轴显著调节卵巢癌血管生成.
这个轴代表了卵巢癌治疗的潜在治疗目标.

关键词:

血管新生的产生.马拉特语马拉特语马拉特语卵巢癌是发生在卵巢中的癌症.在VEGFA中,VEGFA是VEGFA.ceRNARNA是什么意思在 miR-98-3pp

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