Zhejiang Hospital.
Department of General Surgery, Zhejiang Hospital, Hangzhou 310013, China.
Crit Rev Eukaryot Gene Expr. 2024;34(8):25-34. doi: 10.1615/CritRevEukaryotGeneExpr.2024054038.
Lysine demethylase 6A (KDM6A) is abnormally expressed in various cancer. This study aimed to investigate the potential of KDM6A in pancreatic cancer (PC). mRNA expression was calculated by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Protein expression was detected by Western blot. Cell viability was measured by Cell Counting Kit (CCK-8) assay. Cell angiogenesis was determined by tube formation assay. Cell migration and invasion were determined by Transwell assay. We found that KDM6A was upregulated in PC patients and cells. Interestingly, KDM6A deficiency inhibited the proliferation and angiogenesis of PC cells. Moreover, KDM6A knockdown suppressed the migration and invasion of PC cells. Additionally, KDM6A upregulated the expression of lysosomal associated membrane protein 3 (LAMP3) via driving demethylation of H3K27me3. Overexpression of LAMP3 reversed the effects of KDM6A knockdown and contributed to the angiogenesis and aggressiveness of PC cells. In summary, KDM6A-mediated demethylation of tri-methylation at lysine 27 of histone H3 (H3K27me3) promotes the transcription of LAMP3, resulting the angiogenesis and aggressiveness of PC. Therefore, targeting KDM6A may be an anti-angiogenetic strategy for PC.
赖氨酸去甲基化酶 6A(KDM6A)在各种癌症中异常表达。本研究旨在探讨 KDM6A 在胰腺癌(PC)中的潜在作用。通过逆转录定量实时聚合酶链反应(RT-qPCR)计算 mRNA 表达。通过 Western blot 检测蛋白表达。通过细胞计数试剂盒(CCK-8)测定细胞活力。通过管形成测定法测定细胞血管生成。通过 Transwell 测定法测定细胞迁移和侵袭。我们发现 KDM6A 在 PC 患者和细胞中上调。有趣的是,KDM6A 缺失抑制了 PC 细胞的增殖和血管生成。此外,KDM6A 敲低抑制了 PC 细胞的迁移和侵袭。此外,KDM6A 通过驱动组蛋白 H3 第 27 位赖氨酸的三甲基化去甲基化来上调溶酶体相关膜蛋白 3(LAMP3)的表达。LAMP3 的过表达逆转了 KDM6A 敲低的作用,并促进了 PC 细胞的血管生成和侵袭性。总之,KDM6A 介导的组蛋白 H3 第 27 位赖氨酸三甲基化的去甲基化促进了 LAMP3 的转录,导致 PC 的血管生成和侵袭性。因此,靶向 KDM6A 可能是 PC 的一种抗血管生成策略。