Open AccessLCMR1 interacts with DEK to suppress apoptosis in lung cancer cells
Author(s) -
Yang Xu,
Zhixin Liang,
Chunsun Li,
Zhen Yang,
Liangan Chen
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7095
Subject(s) - lung cancer , oncogene , cancer research , biology , carcinogenesis , cell cycle , metastasis , cancer , apoptosis , cell , medicine , pathology , genetics
To win the war against lung cancer, the molecular mechanisms underlying its oncogenesis and metastasis must be identified in order to develop novel diagnosis and treatment strategies. We previously identified a novel gene, namely lung cancer metastasis related protein 1 (LCMR1; GenBank accession no. AY148462), which was demonstrated to be overexpressed in non‑small‑cell lung cancer. LCMR1 expression was significantly associated with clinical stage. To further understand the mechanism of LCMR1 in lung cancer, the present study screened a cDNA library from the lung cancer cell line 95D for proteins interacting with LCMR1 by yeast two‑hybrid assay, and the protein DEK was identified. Co‑immunoprecipitation and glutathione S‑transferase pull‑down assays were performed to confirm the interaction between LCMR1 and DEK in vivo and in vitro. The results demonstrated that the interaction was mediated primarily by the N‑terminal region of DEK, suggesting that LCMR1 may be involved in the regulation of cell apoptosis. Using RNA interference, DEK and LCMR1 were demonstrated to cooperate in the inhibition of apoptosis in lung cancer cells, and this effect was associated with the induced myeloid leukemia protein cell differentiation protein 1 pathway. The present findings suggest that LCMR1 might serve as a potential molecular target for lung cancer therapy.