OncoTargets and Therapy (Feb 2020)

KLF16 Affects the MYC Signature and Tumor Growth in Prostate Cancer

  • Zhang J,
  • Yu W,
  • Wang X,
  • Hu B,
  • Wu D,
  • Shi G

Journal volume & issue
Vol. Volume 13
pp. 1303 – 1310

Abstract

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Jun Zhang,1,2 Wandong Yu,2 Xilong Wang,2 Bo Hu,2 Denglong Wu,1 Guowei Shi2 1Department of Urology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, People’s Republic of China; 2Department of Urology, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai 200240, People’s Republic of ChinaCorrespondence: Guowei ShiDepartment of Urology, The Fifth People’s Hospital of Shanghai, Fudan University, 801 Heqing Road, Minhang District, Shanghai 200240, People’s Republic of ChinaEmail [email protected]: KLF16, a member of the Kruppel-like factor (KLF) family, functions in the regulation of dopaminergic transmission, metabolism, and endocrinology. However, the role of KLF16 in prostate cancer (PCa) remains unknown.Methods: We screened the expression of KLFs in PCa based on bioinformatics analysis. The protein levels of KLF16 in PCa specimens were confirmed by immunohistochemistry. Inhibiting KLF16 by RNA interference with shRNA was used to determine the effects of KLF16 on PCa cell growth in vitro and in vivo. RNA sequencing was used to investigate the signaling regulated by KLF16 in PCa. Bioinformatics analysis was also used to determine the possible correlations of KLF16 and signaling in PCa cohorts.Results: Bioinformatics analysis showed that KLF16 may be required for PCa development. Notably, the expression of KLF16 was elevated in human PCa tissues. In vitro and in vivo experiments both demonstrated that depleting KLF16 significantly inhibited the growth of PCa cells. Downregulation of KLF16 significantly decreased the expression of MYC signaling in PCa cells. Furthermore, KLF16 expression was correlated with MYC signaling activity.Conclusion: KLF16 was overexpressed in PCa tissues compared to normal tissues. KLF16 knockdown suppressed PCa cell growth in vitro and in vivo, and a deficiency of KLF16 inhibited activation of MYC signaling.Keywords: Kruppel-like factor, KLF16, prostate cancer, MYC

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