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2018 ; 9
(51
): 29601-29618
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English Wikipedia
LMO1 functions as an oncogene by regulating TTK expression and correlates with
neuroendocrine differentiation of lung cancer
#MMPMID30038707
Du L
; Zhao Z
; Suraokar M
; Shelton SS
; Ma X
; Hsiao TH
; Minna JD
; Wistuba I
; Pertsemlidis A
Oncotarget
2018[Jul]; 9
(51
): 29601-29618
PMID30038707
show ga
LMO1 encodes a protein containing a cysteine-rich LIM domain involved in
protein-protein interactions. Recent studies have shown that LMO1 functions as an
oncogene in several cancer types, including non-small cell lung cancer (NSCLC).
However, the function of LMO1 in other histological subtypes of lung cancer, such
as small cell lung cancer (SCLC), was not investigated. In analyzing the
expression of LMO1 across a panel of lung cell lines, we found that LMO1
expression levels were significantly and dramatically higher in SCLC cells, an
aggressive neuroendocrine subtype of lung cancer, relative to NSCLC and normal
lung cells. In NSCLC cells, LMO1 mRNA levels were significantly correlated with
expression of neuroendocrine differentiation markers. Our in vitro investigations
indicated that LMO1 had the general property of promoting cell proliferation in
lung cancer cells representing different histological subtypes, suggesting a
general oncogenic function of LMO1 in lung cancer. In investigating the clinical
relevance of LMO1 as an oncogene, we found that a high tumor level of the LMO1
mRNA was an independent predictor of poor patient survival. These results suggest
that LMO1 acts as an oncogene, with expression correlated with neuroendocrine
differentiation of lung cancer, and that it is a determinant of lung cancer
aggressiveness and prognosis. By combining gene expression correlations with
patient survival and functional in vitro investigations, we further identified
TTK as mediating the oncogenic function of LMO1 in lung cancer cells.