HSDL2 Promotes Bladder Cancer Growth In Vitro and In Vivo

Int J Med Sci. 2019 May 7;16(5):654-659. doi: 10.7150/ijms.31288. eCollection 2019.

Abstract

Bladder cancer is a common malignant urinary tumor, and patients with bladder cancer have poor prognosis. Abnormal lipid metabolism in peroxisomes is involved in tumor progression. Hydroxysteroid dehydrogenase-like 2 (HSDL2) localized in peroxisomes regulates fatty acid synthesis. In the present study, we reported that HSDL2 was upregulated in two human bladder cancer cell lines 5637 and T24 compared to normal human urothelial cells. Furthermore, lentiviral-mediated HSDL2 knockdown inhibited the proliferation and colony formation while promoted the apoptosis of human bladder cancer T24 cells in vitro. In nude mice HSDL2 knockdown inhibited the growth of T24 derived xenografts in vivo. In conclusion, our results suggest that HSDL2 plays an oncogenic role in bladder cancer and might serve as a potential target for bladder cancer therapy.

Keywords: HSDL2; apoptosis; bladder cancer; cell proliferation; shRNA.

MeSH terms

  • Animals
  • Apoptosis
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • Hydroxysteroid Dehydrogenases / genetics
  • Hydroxysteroid Dehydrogenases / metabolism*
  • Mice
  • Mice, Nude
  • Oncogenes*
  • RNA, Small Interfering / metabolism
  • Up-Regulation
  • Urinary Bladder / cytology
  • Urinary Bladder / pathology
  • Urinary Bladder Neoplasms / genetics
  • Urinary Bladder Neoplasms / pathology*
  • Urothelium / cytology
  • Urothelium / pathology
  • Xenograft Model Antitumor Assays

Substances

  • RNA, Small Interfering
  • HSDL2 protein, human
  • Hydroxysteroid Dehydrogenases