Neamine inhibits oral cancer progression by suppressing angiogenin-mediated angiogenesis and cancer cell proliferation.

Abstract

BACKGROUND:

Angiogenin undergoes nuclear translocation and stimulates ribosomal RNA transcription in both endothelial and cancer cells. Consequently, angiogenin has a dual effect on cancer progression by inducing both angiogenesis and cancer cell proliferation. The aim of this study was to assess whether neamine, a blocker of nuclear translocation of angiogenin, possesses antitumor activity toward oral cancer.

MATERIALS AND METHODS:

The antitumor effect of neamine on oral cancer cells was examined both in vitro and in vivo.

RESULTS:

Neamine inhibited the proliferation of HSC-2, but not that of SAS oral cancer cells in vitro. Treatment with neamine effectively inhibited growth of HSC-2 and SAS cell xenografts in athymic mice. Neamine treatment resulted in a significant decrease in tumor angiogenesis, accompanied by a decrease in angiogenin- and proliferating cell nuclear antigen-positive cancer cells, especially of HSC-2 tumors.

CONCLUSION:

Neamine effectively inhibits oral cancer progression through inhibition of tumor angiogenesis. Neamine also directly inhibits proliferation of certain types of oral cancer cells. Therefore, neamine has potential as a lead compound for oral cancer therapy.

• Authors: Koji Kishimoto, Shoko Yoshida, Soichiro Ibaragi, Norie Yoshioka, Guo-Fu Hu, Akira Sasaki
• Journal: Anticancer research (Anticancer Res) Vol. 34 Issue 5 Pg. 2113-21 (May 2014) ISSN: 1791-7530 [Electronic] Greece
• PMID: 24778013 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Angiogenesis Inducing Agents
• Framycetin
• neamine
• angiogenin
• Ribonuclease, Pancreatic

Topics

• Angiogenesis Inducing Agents (pharmacology)
• Animals
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Disease Progression
• Framycetin (pharmacology)
• Humans
• Immunohistochemistry
• In Situ Nick-End Labeling
• Mice
• Mice, Nude
• Mouth Neoplasms (blood supply, metabolism, pathology)
• Neovascularization, Pathologic (metabolism, pathology)
• Protein Transport (drug effects)
• Ribonuclease, Pancreatic (metabolism)
• Xenograft Model Antitumor Assays