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2017 ; 108
(6
): 1169-1176
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NUBPL, a novel metastasis-related gene, promotes colorectal carcinoma cell
motility by inducing epithelial-mesenchymal transition
#MMPMID28346728
Wang Y
; Wu N
; Sun D
; Sun H
; Tong D
; Liu D
; Pang B
; Li S
; Wei J
; Dai J
; Liu Y
; Bai J
; Geng J
; Fu S
; Jin Y
Cancer Sci
2017[Jun]; 108
(6
): 1169-1176
PMID28346728
show ga
Nucleotide binding protein-like, NUBPL, is an assembly factor for human
mitochondrial complex I, which is the biggest member of the mitochondrial
respiratory chain. However, the relationship between NUBPL and carcinoma
progression remains unknown. In this study, NUBPL was characterized for its role
in colorectal cancer (CRC) and the underlying molecular mechanisms. Data
(n = 197) from the Oncomine database revealed that mRNA levels of NUBPL were
remarkably overexpressed in CRC tissues compared with normal tissues. In
addition, immunohistochemical analysis of 75 pairs of CRC and non-tumor tissues
showed that the expression level of NUBPL was significantly higher in CRC
tissues, and its expression level was positively associated with lymph node
metastasis (P = 0.028) and advanced staging (P = 0.030). Expression of NUBPL in
metastatic lymph nodes of CRC patients was also detected by immunohistochemical
staining and high expression levels of NUBPL were observed. Overexpression of
NUBPL significantly promoted the migration and invasion ability of CRC cell lines
SW480 and SW620, whereas knockdown of NUBPL lead to an opposite effect. Our
further study found that NUBPL could induce epithelial-mesenchymal transition
(EMT), characterized by downregulation of epithelial markers (E-cadherin) and
upregulation of mesenchymal markers (N-cadherin and vimentin). Moreover, NUBPL
was able to activate ERK, which is believed to promote EMT and tumor metastasis.
Inhibition of ERK suppressed the NUBPL-induced changes in EMT and cell motility.
These data showed that NUBPL plays a vital role in CRC migration and invasion by
inducing EMT and activating ERK. It might be a novel therapeutic target for CRC.
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