Nano-diamino-tetrac (NDAT) inhibits PD-L1 expression which is essential for proliferation in oral cancer cells.

Abstract

Programmed death-ligand 1 (PD-L1) is a critical regulator to defend tumor cells against immune surveillance. Thyroid hormone has been shown to induce PD-L1 expression in cancer cells. Its nano-particulated analogue, nano-diamino-tetrac (NDAT; Nanotetrac) is an anticancer/anti-angiogenic agent. In the current study, the inhibitory mechanism by which NDAT inhibited PD-L1 mRNA abundance and PD-L1 protein content in oral cancer cells was investigated. NDAT inhibited inducible PD-L1 expression and protein accumulation by the inhibition of activated ERK1/2 and PI3K. Knockdown PD-L1 also inhibited the proliferation of oral cancer cells which suggests that the inhibitory effect of NDAT on PD-L1 expression maybe is one of the critical mechanisms for NDAT-induced anti-proliferative effect in oral cancer cells.

• Authors: Shan-Jen Lin, Yu-Tang Chin, Yih Ho, Szu-Yi Chou, Yu-Chen Sh Yang, André Wendindondé Nana, Kuan-Wei Su, Yee-Tong Lim, Kuan Wang, Sheng-Yang Lee, Ya-Jung Shih, Yi-Ru Chen, Jacqueline Whang-Peng, Paul J Davis, Hung-Yun Lin, Earl Fu
• Journal: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association (Food Chem Toxicol) Vol. 120 Pg. 1-11 (Oct 2018) ISSN: 1873-6351 [Electronic] England
• PMID: 29960019 (Publication Type: Journal Article)
• Copyright: Copyright © 2018. Published by Elsevier Ltd.

Chemical References

• Antineoplastic Agents
• B7-H1 Antigen
• CD274 protein, human
• Phosphoinositide-3 Kinase Inhibitors
• Protein Kinase Inhibitors
• RNA, Messenger
• tetraiodothyroacetic acid
• Thyroxine

Topics

• Antineoplastic Agents (pharmacology)
• B7-H1 Antigen (antagonists & inhibitors, genetics, metabolism)
• Carcinoma, Squamous Cell (genetics, metabolism, pathology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Gene Expression (drug effects)
• Gene Knockdown Techniques
• Humans
• MAP Kinase Signaling System (drug effects)
• Mouth Neoplasms (genetics, metabolism, pathology)
• Nanoparticles
• Phosphoinositide-3 Kinase Inhibitors
• Protein Kinase Inhibitors (pharmacology)
• RNA, Messenger (metabolism)
• Thyroxine (analogs & derivatives, pharmacology)