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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Transl+Res
2017 ; 9
(4
): 1708-1719
Nephropedia Template TP
gab.com Text
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English Wikipedia
Inhibition of AMPK-related kinase 5 (ARK5) enhances cisplatin cytotoxicity in
non-small cell lung cancer cells through regulation of epithelial-mesenchymal
transition
#MMPMID28469776
Li M
; Zheng C
; Xu H
; He W
; Ruan Y
; Ma J
; Zheng J
; Ye C
; Li W
Am J Transl Res
2017[]; 9
(4
): 1708-1719
PMID28469776
show ga
Lung cancer incidence and mortality rates are amongst the highest of all
malignant tumors worldwide. ARK5 is a member of the human AMP-activated protein
kinase (AMPK) family which is implicated in tumor survival and progression. The
current study was designed to explore the role of ARK5 in resistance of non-small
cell lung cancer (NSCLC) to cisplatin. We studied the sensitivity of two NSCLC
cell lines, NCI-H1229 and A549, to cisplatin by using proliferation and cell
viability assays. We then examined expression of ARK5, Twist, and the epithelial
to mesenchymal transition (EMT) biomarkers, E-cadherin and Vimentin, by Western
blot and immunofluorescence. We found that ARK5 downregulation significantly
increased the cisplatin chemosensitivity of NSCLC cells, and that NCI-H1299
cells, which express high levels of ARK5 and possess a mesenchymal phenotype,
were more resistant to cisplatin than A549 cells, which show low expression ARK5.
Furthermore, siRNA-mediated silencing of ARK5 resulted in altered EMT patterns in
NSCLC cells. These data support a role for ARK5 in regulating EMT in NSCLC cells.
Together, our findings suggest that ARK5 is a potential drug target for combating
drug resistance and regulating EMT in NSCLC cells.