Abstract
In our previous study, we demonstrated that cyanidin-3-O-glucoside (C3G)-rich haskap (Lonicera caerulea L.) berry extracts can attenuate the carcinogen-induced DNA damage in normal lung epithelial cells in vitro. Here, the efficacy of lyophilized powder of whole haskap berry (C3G-HB) in lowering tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, (NNK)-induced lung tumorigenesis in A/JCr mice was investigated. Three weeks after daily oral administration of C3G-HB (6 mg of C3G in 0.2 g of C3G-HB/mouse/day), lung tumors were initiated by a single intraperitoneal injection of NNK. Dietary C3G-HB supplementation was continued, and 22 weeks later, mice were euthanized. Lung tumors were visualized through positron emission tomography (PET) and magnetic resonance imaging (MRI) 19 weeks after NNK injection. Dietary supplementation of C3G-HB significantly reduced the NNK-induced lung tumor multiplicity and tumor area but did not affect tumor incidence. Immunohistochemical analysis showed reduced expression of proliferative cell nuclear antigen (PCNA) and Ki-67 in lung tissues. Therefore, C3G-HB has the potential to reduce the lung tumorigenesis, and to be used as a source for developing dietary supplements or nutraceuticals for reducing the risk of lung cancer among high-risk populations.
Highlights
Lung cancer is the most commonly diagnosed cancer (11.6% of all the cancers), and the leading cause of cancer deaths (18.4% of all cancer deaths) among both men and women worldwide
We found that C3G-rich whole haskap berry powder (C3G-HB) can suppress NNK-induced lung tumorigenesis in vivo
C3G-HB was rich in minerals, manganese, magnesium, zinc, and copper (Table 1)
Summary
Lung cancer is the most commonly diagnosed cancer (11.6% of all the cancers), and the leading cause of cancer deaths (18.4% of all cancer deaths) among both men and women worldwide. Over 80% of lung cancer incidence is attributed to tobacco smoking [1]. Tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is a known lung carcinogen that causes lung tumors in laboratory animals and is likely to cause lung cancer in humans [2,3]. NNK is converted into reactive electrophilic metabolites, which cause point mutations in critical genes that involve cellular functions. NNK can deregulate the cell cycle, apoptosis, and DNA damage repair [4,5,6]. NNK activates cell growth and proliferation signaling cascades, such as extracellular signal-regulated kinase 1/2 (ERK1/2), mitogen-activated protein kinase (MAPK) [5], and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) [7], resulting in tumorigenesis
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