Premium
ILT4 drives B7‐H3 expression via PI3K/AKT/mTOR signalling and ILT4/B7‐H3 co‐expression correlates with poor prognosis in non‐small cell lung cancer
Author(s) -
Zhang Pei,
Yu Shuwen,
Li Hongyu,
Liu Chuanyong,
Li Juan,
Lin Wenli,
Gao Aiqin,
Wang Linlin,
Gao Wei,
Sun Yuping
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.06.037
Subject(s) - pi3k/akt/mtor pathway , cancer research , immune system , lung cancer , protein kinase b , biology , microbiology and biotechnology , signal transduction , medicine , immunology
Immunoglobulin‐like transcript (ILT) 4 is critical for the inhibitory function of certain immune cells. We previously demonstrated that ILT4 is over‐expressed in human non‐small cell lung cancer (NSCLC) cells and is involved in tumour evasion via an unknown mechanism. In this report, we demonstrate that ILT4 increases the expression of the co‐inhibitory molecule B7‐H3 through PI3K/AKT/mTOR signalling. In primary human NSCLC tissues, a significant positive relationship is observed between ILT4 and B7‐H3 expression. ILT4/B7‐H3 co‐expression is significantly associated with a reduction in T infiltrating lymphoid cells and lower overall survival. In summary, ILT4 increases B7‐H3 expression and ILT4/B7‐H3 co‐expression may be involved in NSCLC progression.