@Article{096504019X15509383469698,
AUTHOR = {Xiangbin Tan, Zefei Liao, Shuangyou Zou, Liangyun Ma, Aimin Wang},
TITLE = {VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin  in Non-Small Cell Lung Cancer via AKT Signaling},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {1},
PAGES = {3--11},
URL = {http://www.techscience.com/or/v28n1/48458},
ISSN = {1555-3906},
ABSTRACT = {Vasohibin2 (VASH2), a proangiogenic factor, has been demonstrated to play an oncogenic role in some 
common human cancers. However, the detailed function of VASH2 in non-small cell lung cancer (NSCLC) has 
not previously been studied. In this study, we found that VASH2 was significantly upregulated in NSCLC tissues 
and cell lines, and its increased expression was associated with NSCLC progression and poor prognosis of 
patients. Knockdown of VASH2 markedly inhibited cell proliferation and P-glycoprotein expression in NSCLC 
cells. Overexpression of VASH2 enhanced cell proliferation, P-glycoprotein expression, as well as doxorubicin 
resistance in NSCLC cells. Moreover, the expression levels of VASH2 were significantly increased in newly 
established doxorubicin-resistant NSCLC cells. Molecular mechanism investigation revealed that inhibition of 
VASH2 expression in NSCLC cells suppressed the activity of AKT signaling, and overexpression of VASH2 
enhanced the activity of AKT signaling. We further showed that downregulation of AKT signaling activity 
using AKT inhibitor LY294002 markedly inhibited NSCLC cell proliferation and resistance to doxorubicin 
induced by VASH2. In conclusion, the findings in the present study indicate that VASH2 promotes NSCLC cell 
proliferation and resistance to doxorubicin via modulation of AKT signaling. Thus, we suggest that VASH2 
may become a potential therapeutic target for the treatment of NSCLC.},
DOI = {10.3727/096504019X15509383469698}
}