Hydrogen Sulfide-Releasing Carbonic Anhydrase Inhibitors Effectively Suppress Cancer Cell Growth

Int J Mol Sci. 2024 Sep 17;25(18):10006. doi: 10.3390/ijms251810006.

Abstract

This study proposes a novel therapeutic strategy for cancer management by combining the antitumor effects of hydrogen sulfide (H2S) and inhibition of carbonic anhydrases (CAs; EC 4.2.1.1), specifically isoforms IV, IX, and XII. H2S has demonstrated cytotoxicity against various cancers at high concentrations. The inhibition of tumor-associated CAs leads to lethal intracellular alkalinization and acidification of the extracellular tumor microenvironment and restores tumor responsiveness to the immune system, chemotherapy, and radiotherapy. The study proposes H2S donor-CA inhibitor (CAI) hybrids for tumor management. These compounds effectively inhibit the target CAs, release H2S consistently, and exhibit potent antitumor effects against MDA-MB-231, HCT-116, and A549 cancer cell lines. Notably, some compounds display high cytotoxicity across all investigated cell lines. Derivative 30 shows a 2-fold increase in cytotoxicity (0.93 ± 0.02 µM) under chemically induced hypoxia in HCT-116 cells. These compounds also disturb the cell cycle, leading to a reduction in cell populations in G0/G1 and S phases, with a notable increase in G2/M and Sub-G1. This disruption is correlated with induced apoptosis, with fold increases of 37.2, 24.5, and 32.9 against HCT-116 cells and 14.2, 13.1, and 19.9 against A549 cells compared to untreated cells. These findings suggest the potential of H2S releaser-CAI hybrids as effective and versatile tools in cancer treatment.

Keywords: antitumor; cancer; carbonic anhydrase; donor; hybrid; hydrogen sulfide; in vitro; inhibitor; multitarget; tumor.

MeSH terms

  • A549 Cells
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology
  • Apoptosis* / drug effects
  • Carbonic Anhydrase Inhibitors* / chemistry
  • Carbonic Anhydrase Inhibitors* / pharmacology
  • Carbonic Anhydrases / metabolism
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation* / drug effects
  • HCT116 Cells
  • Humans
  • Hydrogen Sulfide* / chemistry
  • Hydrogen Sulfide* / metabolism
  • Hydrogen Sulfide* / pharmacology
  • Neoplasms / drug therapy
  • Neoplasms / metabolism
  • Neoplasms / pathology

Substances

  • Hydrogen Sulfide
  • Carbonic Anhydrase Inhibitors
  • Antineoplastic Agents
  • Carbonic Anhydrases

Grants and funding

This research received no external funding.