Blockers of Nicotinic Acetylcholine Receptors Delay Tumor Growth and Increase Antitumor Activity of Mouse Splenocytes

Dokl Biochem Biophys. 2020 Mar;491(1):89-92. doi: 10.1134/S1607672920020143. Epub 2020 Jun 1.

Abstract

Blockade of α6, α3β2, α9α10, and α7 subtypes of nicotinic acetylcholine receptors slows tumor growth in vivo, increases cytotoxic activity of splenocytes from tumor-bearing mice, and, to some extent, reduces the viability of Ehrlich carcinoma cells in vitro. These data indicate that nicotinic acetylcholine receptors are involved in oncogenesis, affecting the survival of tumor cells, inter alia, via modulation of the antitumor immunity.

Keywords: Ehrlich carcinoma; neurotoxins; nicotinic receptors; splenocytes.

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology*
  • Carcinogenesis
  • Carcinoma, Ehrlich Tumor / metabolism*
  • Cell Proliferation
  • Cell Survival
  • Conotoxins / metabolism
  • Mice
  • Neoplasm Transplantation
  • Nicotinic Antagonists / chemistry
  • Nicotinic Antagonists / pharmacology*
  • Receptors, Nicotinic / metabolism
  • Spleen / cytology*
  • alpha7 Nicotinic Acetylcholine Receptor / antagonists & inhibitors

Substances

  • Antineoplastic Agents
  • Chrna9 protein, mouse
  • Conotoxins
  • Nicotinic Antagonists
  • Receptors, Nicotinic
  • alpha7 Nicotinic Acetylcholine Receptor
  • nicotinic receptor alpha3beta2
  • nicotinic receptor alpha6