Figure 1: Tumor growth and invasion in celecoxib (Ce) or vehicle-treated mice exposed to normoxia (N) or intermittent hypoxia (IH). | Scientific Reports

Figure 1: Tumor growth and invasion in celecoxib (Ce) or vehicle-treated mice exposed to normoxia (N) or intermittent hypoxia (IH).

From: Role of Cyclooxygenase-2 on Intermittent Hypoxia-Induced Lung Tumor Malignancy in a Mouse Model of Sleep Apnea

Figure 1

(a) Periodic tumor volume measurements revealed an accelerated tumor growth in IH-treated mice compared to N, which was inhibited by Ce administration. (b) Weight average of tumors from mice exposed to IH experienced ~2-fold increase respect to N. Under IH conditions, daily administration of Ce promoted a markedly reduction in tumor weight. (c) Representative histological sections of the tumor and the adjacent muscle presenting non-invasion (left) or invasion (right). LLC1 cells are predominantly stained by hematoxylin (dark blue, yellow arrows) whereas myocytes are more intensely stained with eosin (pink, white arrows). Scale bar = 100 μm. The number of mice presenting invasion was higher in IH vs N exposed mice. (d) Number of lung metastases, mean size, and relative metastatic area do not exhibit significant variations among the different treatments due to a high intra-group variability. Representative image of a metastasis (yellow arrow) in the lung parenchyma. Scale bar = 100 μm. Tumors (e) and purified TAMs (f) from IH-exposed mice showed a trend to an increased COX-2 protein and PTGS2 gene relative expression, respectively. (g) LLC1 proliferation in response to exogenous PGE2 in vitro. Data are presented as mean ± SE.

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