Therapeutic potential of endogenous hydrogen sulfide inhibition in breast cancer (Review)

Oncol Rep. 2021 May;45(5):68. doi: 10.3892/or.2021.8019. Epub 2021 Mar 24.

Abstract

Hydrogen sulfide (H2S), the third gas signal molecule, is associated with the modulation of various physiological and pathological processes. Recent studies have reevealed that endogenous H2S may promote proliferation, induce angiogenesis and inhibit apoptosis, thereby stimulating oncogenesis. Conversely, decreased endogenous H2S release suppresses growth of various tumors including breast cancer. This observation suggests an alternative tumor therapy strategy by inhibiting H2S‑producing enzymes to reduce the release of endogenous H2S. Breast cancer is the most common type of cancer in women. Due to the lack of approved targeted therapy, its recurrence and metastasis still affect its clinical treatment. In recent years, significant progress has been made in the control of breast cancer by using inhibitors on H2S‑producing enzymes. This review summarized the roles of endogenous H2S‑producing enzymes in breast cancer and the effects of the enzyme inhibitors on anticancer and anti‑metastasis, with the aim of providing new insights for the treatment of breast cancer.

Keywords: breast cancer; endogenous hydrogen sulfide; anticancer effect.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / pathology
  • Carcinogenesis / drug effects
  • Carcinogenesis / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cystathionine beta-Synthase / antagonists & inhibitors
  • Cystathionine beta-Synthase / metabolism
  • Cystathionine gamma-Lyase / antagonists & inhibitors
  • Cystathionine gamma-Lyase / metabolism
  • Enzyme Inhibitors / pharmacology*
  • Enzyme Inhibitors / therapeutic use
  • Female
  • Humans
  • Hydrogen Sulfide / antagonists & inhibitors*
  • Hydrogen Sulfide / metabolism
  • Mice
  • Neovascularization, Pathologic / drug therapy*
  • Neovascularization, Pathologic / pathology
  • Signal Transduction / drug effects
  • Sulfurtransferases / antagonists & inhibitors
  • Sulfurtransferases / metabolism
  • Xenograft Model Antitumor Assays

Substances

  • Enzyme Inhibitors
  • Sulfurtransferases
  • 3-mercaptopyruvate sulphurtransferase
  • Cystathionine beta-Synthase
  • Cystathionine gamma-Lyase
  • Hydrogen Sulfide

Grants and funding

The present study was supported by grants from the National Natural Science Foundation of China (grant no. 82072726), as well as the Natural Science Foundation of Henan Province in China (grant no. 202300410079).