Department of Infectious Diseases, the First Affiliated Hospital of Xi'an Jiaotong University, Yanta West Road No. 277, Xi'an 710061, China.
Department of Hematology, the Second Affiliated Hospital of Xi'an Jiaotong University, West Five Road No. 157, Xi'an 710004, China.
Int J Biol Sci. 2020 May 15;16(12):2063-2071. doi: 10.7150/ijbs.45999. eCollection 2020.
Krüppel-like factor 10 (KLF10) has been identified as an important regulator in carcinogenesis and cancer progression. However, the role of KLF10 in multiply myeloma (MM) development and progression remains unknown. In present study, we found that KLF10 mRNA and protein were down-regulated in MM tissues and cell lines. Notably, KLF10 inhibited cell proliferation, cell cycle progression and promoted apoptosis and . Furthermore, we confirmed that KLF10 inhibited β-catenin nuclear translocation and inhibited PTTG1 transcription. PTTG1 knockdown could mimic the biological effects of KLF10. Moreover, we demonstrated that KLF10 expression was regulated by miR-106b-5p. In MM tissues, miR-106b-5p has an inverse correlation with KLF10 expression. Conclusively, our results demonstrated that KLF10 functions as a tumor suppressor in regulating tumor growth of MM under regulation of miR-106b-5p, supporting its potential therapeutic target for MM.
Krüppel 样因子 10（KLF10）已被确定为致癌和癌症进展中的重要调节因子。然而，KLF10 在多发性骨髓瘤（MM）发生和发展中的作用仍不清楚。在本研究中，我们发现 KLF10 mRNA 和蛋白在 MM 组织和细胞系中下调。值得注意的是，KLF10 抑制细胞增殖、细胞周期进程，并促进凋亡。此外，我们证实 KLF10 抑制β-连环蛋白核易位并抑制 PTTG1 转录。PTTG1 敲低可以模拟 KLF10 的生物学效应。此外，我们证明 KLF10 的表达受 miR-106b-5p 调控。在 MM 组织中，miR-106b-5p 与 KLF10 的表达呈负相关。总之，我们的研究结果表明，KLF10 作为一种肿瘤抑制因子，通过 miR-106b-5p 调控 MM 肿瘤生长，支持其作为 MM 的潜在治疗靶点。
