scholarly journals Inhibition of lung tumor development by berry extracts in mice exposed to cigarette smoke

2012 ◽  
Vol 131 (9) ◽  
pp. 1991-1997 ◽  
Author(s):  
Roumen Balansky ◽  
Gancho Ganchev ◽  
Marietta Iltcheva ◽  
Maria Kratchanova ◽  
Petko Denev ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Tumor ◽  
Tumor Development ◽  
Berry Extracts

Chemopreventive Potential of α-Carotene Against Mouse Liver and Lung Tumor Development: Comparison with β-Carotene and α-Tocopherol

1997 ◽  
pp. 529-532 ◽  
Author(s):  
Hiroyuki Tsuda ◽  
Yoshio Iwahori ◽  
Takaaki Hori ◽  
Makoto Asamoto ◽  
Hiroyasu Baba-Toriyama ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Lung Tumor ◽  
Tumor Development ◽  
Β Carotene

scholarly journals Decreased Lung Tumor Development in SwAPP Mice through the Downregulation of CHI3L1 and STAT 3 Activity via the Upregulation of miRNA342-3p

2019 ◽  
Vol 16 ◽  
pp. 63-72 ◽  
Author(s):  
Dong Hun Lee ◽  
Ki Cheon Kim ◽  
Chul Ju Hwang ◽  
Kyung Ran Park ◽  
Young Suk Jung ◽  
...  
Keyword(s):  
Lung Tumor ◽  
Tumor Development

scholarly journals Systems toxicology approaches enable mechanistic comparison of spontaneous and cigarette smoke-related lung tumor development in the A/J mouse model

2014 ◽  
Vol 7 (2) ◽  
pp. 73-84 ◽  
Author(s):  
Karsta Luettich ◽  
Yang Xiang ◽  
Anita Iskandar ◽  
Alain Sewer ◽  
Florian Martin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Cigarette Smoke ◽  
Lung Tumor ◽  
Immune Surveillance ◽  
Gene Expression Signature ◽  
Chemical Carcinogenesis ◽  
Lung Tumors ◽  
Whole Body ◽  
Significant Differential Expression

ABSTRACT The A/J mouse is highly susceptible to lung tumor induction and has been widely used as a screening model in carcinogenicity testing and chemoprevention studies. However, the A/J mouse model has several disadvantages. Most notably, it develops lung tumors spontaneously. Moreover, there is a considerable gap in our understanding of the underlying mechanisms of pulmonary chemical carcinogenesis in the A/J mouse. Therefore, we examined the differences between spontaneous and cigarette smokerelated lung tumors in the A/J mouse model using mRNA and microRNA (miRNA) profiling. Male A/J mice were exposed whole-body to mainstream cigarette smoke (MS) for 18 months. Gene expression interaction term analysis of lung tumors and surrounding nontumorous parenchyma samples from animals that were exposed to either 300 mg/m3 MS or sham-exposed to fresh air indicated significant differential expression of 296 genes. Ingenuity Pathway Analysis® (IPA®) indicated an overall suppression of the humoral immune response, which was accompanied by a disruption of sphingolipid and glycosaminoglycan metabolism and a deregulation of potentially oncogenic miRNA in tumors of MS-exposed A/J mice. Thus, we propose that MS exposure leads to severe perturbations in pathways essential for tumor recognition by the immune system, thereby potentiating the ability of tumor cells to escape from immune surveillance. Further, exposure to MS appeared to affect expression of miRNA, which have previously been implicated in carcinogenesis and are thought to contribute to tumor progression. Finally, we identified a 50-gene expression signature and show its utility in distinguishing between cigarette smoke-related and spontaneous lung tumors

The Effects of Dietary Myoinositol on Lung Tumor Development in Tobacco Smoke-Exposed Mice

2004 ◽  
Vol 16 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Hanspeter Witschi ◽  
Imelda Espiritu ◽  
Man Ly ◽  
Dale Uyeminami
Keyword(s):  
Tobacco Smoke ◽  
Lung Tumor ◽  
Tumor Development

Enhancement of N-bis(2-hydroxypropyl)nitrosamine-initiated lung tumor development in rats by bleomycin and N-methyl-N-nitrosourethane

1984 ◽  
Vol 25 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Tomoyuki Shirai ◽  
Atsuko Masuda ◽  
Masao Hirose ◽  
Etsuo Ikawa ◽  
Nobuyuki Ito
Keyword(s):  
Lung Tumor ◽  
Tumor Development

scholarly journals Overexpression of PRDX4 Modulates Tumor Microenvironment and Promotes Urethane-Induced Lung Tumorigenesis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jianbo Zheng ◽  
Xin Guo ◽  
Yuka Nakamura ◽  
Xiaolei Zhou ◽  
Reimon Yamaguchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Lung Tumor ◽  
Interleukin 1 ◽  
Tumor Development ◽  
Tumor Model ◽  
Tumor Formation ◽  
Tumor Diameter

Peroxiredoxin 4 (PRDX4), initially reported as an antioxidant, is overexpressed in lung cancer and participates in its progression. However, its role in the urethane-induced lung tumor model is undetermined. The aim of this study was to investigate the effect of PRDX4 overexpression on carcinogen-induced lung tumor development. Human PRDX4 overexpression transgenic (Tg) mice (hPRDX4+/+) and non-Tg mice were intraperitoneally injected with urethane to induce lung tumor. After 6 months, tumor formation was compared between groups and possible mechanisms for the difference in tumor development were investigated. The serum and lung PRDX4 expressions were enhanced after urethane stimulation in Tg mice. Both the average number of tumors (≥0.5 mm) and tumor diameter per mouse in the Tg group were significantly larger than in non-Tg controls, while body weight was lower in the Tg group. Compared with non-Tg controls, tumor cell proliferation was enhanced, while tumor cell apoptosis was suppressed in Tg mice. Systemic oxidative stress and oxidative stress in lung tumors were inhibited by PRDX4 overexpression. The balance of prooxidant enzymes and antioxidant enzymes was also shifted to a decreased level in Tg tumor. In lung tumor tissue, the density of microvessel penetrated into tumor was higher in the Tg group; macrophage infiltration was enhanced in Tg tumors, while there was no difference in T lymphocyte infiltration; the expressions of cytokines, including interleukin-1 beta (IL-1β) and matrix metallopeptidase 9 (MMP9), were elevated in Tg tumors, which resulted from enhanced phosphorylation of nuclear factor-κB p65 (NF-κB p65) and c-Jun, respectively. In conclusion, PRDX4 overexpression modulated tumor microenvironment and promoted tumor development in the mouse urethane-induced lung cancer model.

scholarly journals Dexmedetomidine Associated Lung Cancer Proliferation and Tumor Growth is Prevented by β-Caryophyllene: Role of AMPK Activation and PGC-1α/TFAM Over Expression

2022 ◽  
Author(s):  
Dan Wang ◽  
Dazhi Long ◽  
Jiegang Zhou ◽  
Ziqiang Dong ◽  
Guiming Huang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Lung Tumor ◽  
Apoptotic Cell ◽  
Tumor Development ◽  
A549 Cells ◽  
Treated Group ◽  
Metastatic Progression ◽  
Cancer Proliferation

Background: Dexmedetomidine has been reported to induce anti-apoptotic effects and metastatic progression in lung cancer. In the current investigation, the effect of β-Caryophyllene on dexmedetomidine induced cell proliferation and apoptosis of lung cancer cells and tumor growth in mice was studied. Methods: A549 cell line was cultured with either dexmedetomidine alone or together with β-Caryophyllene for 24 h and analysed for cell proliferation with MTT assay. ELISA based kit was used to determine apoptotic DNA fragmentation. Western blotting was used to determine expression levels of target proteins. The induction of experimental lung tumor in rat model was achieved through the injection of A549 tumor cells subcutaneously into the middle left side of the mice after anesthetization with pentobarbital (35 mg/kg) at 2.8 × 106 cells in 400 μl of PBS. Result: We found that β-Caryophyllene exerts the anti-proliferative effects on A549 cells. Furthermore, β-Caryophyllene significantly prevents apoptotic cell death and causes up-regulation of PGC-1α and TFAM compared to dexmedetomidine treated cells. We observed that β-Caryophyllene suppressed tumor development in mice significantly compared to dexmedetomidine treated group without changing body weight.

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