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 in vitro and in vivo. 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.

中文翻译：

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KLF10 在 microRNA-106b-5p 的调控下通过调节多发性骨髓瘤中的 PTTG1 来抑制细胞生长。

Krüppel 样因子 10 (KLF10) 已被确定为致癌和癌症进展的重要调节因子。然而，KLF10 在多发性骨髓瘤 (MM) 发展和进展中的作用仍然未知。在本研究中，我们发现 KLF10 mRNA 和蛋白质在 MM 组织和细胞系中下调。值得注意的是，KLF10 在体外和体内抑制细胞增殖、细胞周期进程并促进细胞凋亡。此外，我们证实 KLF10 抑制 β-连环蛋白核转位并抑制 PTTG1 转录。PTTG1 敲低可以模拟 KLF10 的生物学效应。此外，我们证明了 KLF10 的表达受 miR-106b-5p 的调节。在 MM 组织中，miR-106b-5p 与 KLF10 表达呈负相关。最终，