Open Access
ARTICLE
VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin in Non-Small Cell Lung Cancer via AKT Signaling
Xiangbin Tan*1, Zefei Liao†1, Shuangyou Zou*, Liangyun Ma†, Aimin Wang*
* Department of Oncology, No. 175 Hospital of People’s Liberation Army, Zhangzhou, Fujian, P.R. China
† Department of Thoracic Surgery, No. 180 Hospital of People’s Liberation Army, Quanzhou, Fujian, P.R. China
Oncology Research 2020, 28(1), 3-11. https://doi.org/10.3727/096504019X15509383469698
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.
Keywords
Cite This Article
Tan, X., Liao, Z., Zou, S., Ma, L., Wang, A. (2020). VASH2 Promotes Cell Proliferation and Resistance to Doxorubicin in Non-Small Cell Lung Cancer via AKT Signaling.
Oncology Research, 28(1), 3–11. https://doi.org/10.3727/096504019X15509383469698