Oncotarget

Research Papers:

Oral kanglaite injection (KLTI) attenuates the lung cancer-promoting effect of high-fat diet (HFD)-induced obesity

Ning Cao, Xiaofang Ma, Zhenzhen Guo, Yaqiu Zheng, Shengnan Geng, Mingjing Meng, Zhenhua Du, Haihong Lin, Yongjian Duan and Gangjun Du _

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Oncotarget. 2016; 7:61093-61106. https://doi.org/10.18632/oncotarget.11212

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Abstract

Ning Cao1,*, Xiaofang Ma1,*, Zhenzhen Guo1, Yaqiu Zheng1, Shengnan Geng1, Mingjing Meng1, Zhenhua Du1, Haihong Lin1, Yongjian Duan2, Gangjun Du1

1Institute of Pharmacy, Pharmacy College of Henan University, Jinming District, Kaifeng, Henan Province 475004, China

2Department of Oncology, The First Hospital Affiliated to Henan University, Kaifeng, Henan Province 475001, China

*These authors contributed equally to this work

Correspondence to:

Gangjun Du, email: [email protected]

Haihong Lin, email: [email protected]

Keywords: kanglaite injection (KLTI), overweight and obesity, metabolic dysfunction, cellular signaling molecules, tissue edema

Received: June 11, 2016     Accepted: July 30, 2016     Published: August 11, 2016

ABSTRACT

Obesity is a risk factor for cancer and cancer-related mortality, however, its role in lung cancer progression remains controversial. This study aimed to assess whether high-fat diet (HFD)-induced obesity promotes lung cancer progression and whether the promotion can be decreased by Kanglaite injection (KLTI). In vivo, HFD-induced overweight or obesity increases the lung carcinoma incidence and multiplicity in a urethane-induced lung carcinogenic model and cancer-related mortality in a LLC allograft model by increasing oxidative stress and cellular signaling molecules including JAK, STAT3, Akt, mTOR, NF-κB and cyclin D1. These changes resulted in increases in vascular disruption and the lung water content, thereby promoting lung epithelial proliferation and the epithelial-mesenchymal transition (EMT) during carcinogenesis. Chronic KLTI treatment substantially prevented the weight gain resulting from HFD consumption, thereby reversing the metabolic dysfunction-related physiological changes and reducing susceptibility to lung carcinogenesis. In vitro, KLTI significantly suppressed the proliferation and induced apoptosis and differentiation in 3T3-L1 preadipocyte cells and attenuated endothelial cell permeability in HUVECs. Our study indicates that there is a potential relationship between obesity and lung cancer. This is the first study to show that obesity can directly accelerate carcinogen-induced lung cancer progression and that KLTI can decrease the lung cancer-promoting effect of HFD-induced obesity.


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