ISSN 1004-6879

CN 13-1154/R

 

承德医学院学报 ›› 2026, Vol. 43 ›› Issue (1): 1-6.

• 基础医学 •    下一篇

LncRNA MITA1靶向miR-30b-3p对肝细胞癌细胞生物学活性的影响

金雯1, 李群1, 王波2,*, 周健坤2, 张俊2, 曹立宇3   

  1. 1.铜陵职业技术学院医学系,安徽 铜陵 244061;
    2.铜陵职业技术学院护理系,安徽 铜陵 244061;
    3.安徽医科大学附属阜阳医院病理科,安徽 阜阳 236000
  • 收稿日期:2024-12-06 出版日期:2026-02-10 发布日期:2026-02-12
  • 通讯作者: *王波(1983—),男,教授,研究方向:肝癌生物学机制;E-mail:117516079@qq.com。
  • 作者简介:金雯(1982—),女,硕士,副教授,研究方向:肝癌发病机制。
  • 基金资助:
    安徽高校自然科学研究重点项目(2024AH051863)

Effect of LncRNA MITA1 targeting miR-30b-3p on biological behavior of hepatocellular carcinoma cells

JIN Wen1, LI Qun1, WANG Bo2,*, ZHOU Jiankun2, ZHANG Jun2, CAO Liyu3   

  1. 1. Department of Medical, Tongling Polytechnic College, Tongling, Anhui, 244061, China;
    2. Department of Nursing, Tongling Polytechnic College, Tongling, Anhui, 244061, China;
    3. Department of Pathology, Fuyang Hospital Affiliated to Anhui Medical University, Fuyang, Anhui, 236000, China
  • Received:2024-12-06 Online:2026-02-10 Published:2026-02-12

摘要: 目的 探究LncRNA MITA1在肝细胞癌(HCC)发展中的作用机制。方法 采用qRT-PCR检测HCC组织及细胞内MITA1 mRNA的表达;采用pcDNA3.1重组质粒载体过表达MITA1。SMMC7721细胞处理后分别标记为空白组、OE-MITA1-NC组、OE-MITA1组。平板克隆实验检测细胞增殖;Transwell检测细胞侵袭;细胞计数试剂盒-8(CCK-8)检测细胞活力;免疫印迹法检测Vimentin、MMP-2、N-Cadherin蛋白表达;双荧光素酶报告实验验证MITA1和miR-30b-3p的靶向关系。结果 与癌周正常肝组织相比,HCC组织及细胞内MITA1 mRNA含量呈高表达,而miR-30b-3p mRNA呈低表达(P<0.05);MITA1过表达下,OE-MITA1组MITA1 mRNA表达水平升高(P<0.05)。与空白组和OE-MITA1-NC组相比,OE-MITA1组细胞增殖和侵袭数量增加且细胞活性增强(P<0.05);Vimentin、MMP-2、N-Cadherin蛋白表达升高(P<0.05)。双荧光素酶报告显示,MITA1与miR-30b-3p之间具有靶向关系,且MITA1与miR-30b-3p表达呈负调控关系。结论 LncRNA MITA1通过绑定miR-30b-3p调控并促进HCC细胞的增殖、侵袭和细胞活力,可作为HCC诊疗潜在的靶点。

关键词: 长链非编码RNA MITA1, miR-30b-3p, 肝细胞癌, 增殖, 侵袭

Abstract: Objective To investigate the mechanistic role of LncRNA MITA1 in the progression of hepatocellular carcinoma (HCC). Methods qRT-PCR was employed to assess the expression levels of MITA1 mRNA in HCC tissues and cells. The pcDNA3.1 recombinant plasmid vector was utilized to overexpress MITA1. After treatment, SMMC7721 cells were categorized into three groups, the normal group, the OE-MITA1-NC (negative control) group, and the OE-MITA1 (overexpression) group. Cell proliferation was evaluated using a colony formation assay, while cell invasion was assessed via the Transwell assay. Cell viability was determined using the Cell Counting Kit-8 (CCK-8) assay. Protein expression levels of Vimentin, MMP-2, and N-Cadherin were measured by western blotting. Additionally, the dual-luciferase reporter assay was conducted to verify the targeting relationship between MITA1 and miR-30b-3p. Results Compared with adjacent normal liver tissues, HCC tissues and cells exhibited significantly higher expression levels of MITA1 mRNA and lower expression levels of miR-30b-3p mRNA (P<0.05). Under MITA1 overexpression conditions, the OE-MITA1 group demonstrated elevated MITA1 mRNA expression levels (P<0.05). Compared with the normal and OE-MITA1-NC groups, the OE-MITA1 group exhibited increased cell proliferation, invasion capacity, and enhanced cell viability (P<0.05). Furthermore, protein expression levels of Vimentin, MMP-2, and N-Cadherin were significantly higher in the OE-MITA1 group compared with the other two groups (P<0.05). The dual-luciferase reporter assay confirmed a targeting relationship between MITA1 and miR-30b-3p, with MITA1 expression negatively regulating miR-30b-3p expression. Conclusion LncRNA MITA1 can promotes the proliferation, invasion and cell activity of liver cancer by binding miR-30b-3p, MITA1 may serve as a potential therapeutic target for the diagnosis and treatment of HCC.

Key words: LncRNA MITA1, miR-30b-3p, hepatocellular carcinoma, proliferation, invasion

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