| 黄丽,龚豪,胡珊,龚坤雪.BCKDK通过激活Wnt/β-catenin信号通路调控子宫内膜癌细胞的增殖与凋亡.[J].中南医学科学杂志.,2026,(1):39-43, 90. |
| BCKDK通过激活Wnt/β-catenin信号通路调控子宫内膜癌细胞的增殖与凋亡 |
| Branched-chain alpha-keto acid dehydrogenase kinase regulates proliferation and apoptosis of endometrial cancer cells via activating Wnt/β-catenin signaling pathway |
| 投稿时间：2025-04-30 修订日期：2025-11-22 |
| DOI：10.15972/j.cnki.43-1509/r.2026.01.008 |
| 中文关键词: BCKDK 子宫内膜癌 细胞增殖 细胞凋亡 Wnt/β-catenin信号通路 |
| 英文关键词:branched-chain α-keto acid dehydrogenase kinase endometrial neoplasms cell proliferation apoptosis Wnt/β-catenin signaling pathway |
| 基金项目:十堰市科技局引导性项目(22Y41、21Y22) 作者简介:黄丽,硕士,主治医师,研究方向为妇科肿瘤,E-mail为awdd20220415@163.com。 |
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| 中文摘要: |
| 目的探究支链α-酮酸脱氢酶激酶(BCKDK)基于Wnt/β-catenin信号通路对子宫内膜癌细胞增殖、凋亡的影响。 方法采用实时定量PCR和Western blotting法分别检测子宫内膜癌组织与癌旁组织、正常人子宫内膜上皮细胞以及子宫内膜癌细胞系HEC-1-A和Ishikawa中BCKDK的表达水平。通过慢病毒感染技术构建BCKDK低表达的子宫内膜癌细胞模型,并采用CCK-8法分析细胞活力,流式细胞术检测细胞凋亡情况,Western blotting法检测CyclinD1、CDK2、caspase-3、caspase-9、Wnt3a及β-catenin等蛋白表达水平。进一步在BCKDK低表达细胞中加入Wnt/β-catenin信号通路激活剂LiCl,观察其对BCKDK抑制所引起的细胞增殖和凋亡的影响。 结果子宫内膜癌组织BCKDK mRNA表达水平高于癌旁组织(P＜0.05)。不同分化程度、临床分期及淋巴结转移的子宫内膜癌组织中BCKDK mRNA水平比较,差异有显著性(P＜0.05)。与正常人子宫内膜上皮细胞相比,HEC-1-A和Ishikawa两种子宫内膜癌细胞系中BCKDK蛋白及mRNA表达均明显上调(P＜0.05)。与阴性对照组相比,shBCKDK组的BCKDK蛋白和mRNA表达、细胞活力、CyclinD1与CDK2蛋白表达、Wnt3a和β-catenin蛋白表达均显著降低,细胞凋亡率、caspase-3和caspase-9蛋白表达则显著升高；而在加入LiCl激活Wnt/β-catenin通路后,shBCKDK+LiCl组的上述所有指标变化均较shBCKDK组出现显著逆转(P＜0.05)。 结论BCKDK在子宫内膜癌细胞表达异常升高,下调BCKDK表达可抑制HEC-1-A、Ishikawa细胞增殖,并促进其凋亡,其机制可能与调节Wnt/β-catenin信号通路有关。 |
| 英文摘要: |
| AimTo investigate the effect of branched-chain α-keto acid dehydrogenase kinase (BCKDK) on the proliferation and apoptosis of endometrial cancer cells through the Wnt/β-catenin signaling pathway. MethodsThe mRNA and protein expression levels of BCKDK in endometrial cancer tissues, adjacent normal tissues, normal endometrial epithelial cells, and endometrial cancer cell lines (HEC-1-A and Ishikawa) were detected by quantitative real-time PCR and Western blotting. A BCKDK-knockdown endometrial cancer cell model was established using lentiviral infection. Cell viability was analyzed by CCK-8 assay, apoptosis was detected by flow cytometry, and the protein expression levels of CyclinD1, CDK2, caspase-3, caspase-9, Wnt3a, and β-catenin were measured by Western blotting. The Wnt/β-catenin signaling pathway activator LiCl was added to BCKDK-knockdown cells to observe its effect on proliferation and apoptosis. ResultsBCKDK mRNA expression was significantly higher in endometrial cancer tissues than that in adjacent normal tissues (P＜0.05). BCKDK mRNA levels varied significantly with tumor differentiation, clinical stage, and lymph node metastasis (P＜0.05). Both HEC-1-A and Ishikawa cell lines showed significantly elevated BCKDK mRNA and protein expression compared with normal endometrial epithelial cells (P＜0.05). Compared with the negative control group, the shBCKDK group exhibited decreased BCKDK expression, cell viability, CyclinD1, CDK2, Wnt3a, and β-catenin protein levels, as well as increased apoptosis and elevated caspase-3 and caspase-9 expression. However, these effects were significantly reversed by LiCl treatment in the shBCKDK+LiCl group (P＜0.05). ConclusionBCKDK is highly expressed in endometrial cancer cells. Downregulation of BCKDK inhibits proliferation and promotes apoptosis of HEC-1-A and Ishikawa cells, possibly through the regulation of Wnt/β-catenin signaling pathway. |
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