KLF10 inhibits cell growth by regulating PTTG1 in multiple myeloma under the regulation of microRNA-106b-5p

  • Mimi Zhou
  • , Jinqiu Chen
  • , Hui Zhang
  • , Hailing Liu
  • , Huan Yao
  • , Xiaman Wang
  • , Wanggang Zhang
  • , Yingren Zhao
  • , Nan Yang

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)2063-2071
Number of pages9
JournalInternational Journal of Biological Sciences
Volume16
Issue number12
DOIs
StatePublished - 2020
Externally publishedYes

Keywords

  • KLF10
  • MiR-106b-5p
  • Multiply myeloma
  • PTTG1
  • Proliferation

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