Table 2 FOXM1 transgenic mouse models used in the study of pulmonary diseases
Mouse models | Expression of FOXM1 | Cells | Consequences of the models | Reference |
|---|---|---|---|---|
Mx-Cre FOXM1−/− mice | Deletion | All cell types | 60% reduction in medium-sized (0.5–1 mm) lung adenomas; no large lung adenomas > 1 mm in size;84% of lung tumors exhibited strong FOXM1 nuclear positivity; 16% FOXM1-negative tumors were significantly smaller in size | [25] |
Rosa26-FOXM1 transgenic mice | Overexpression | All cell types | Persistent pulmonary inflammation increased the total number and diameter of lung adenomas | [44] |
SPC–rtTAtg/−/ TetO-Cretg/−/FOXM1fl/fl mice termed epFOXM1−/− mice, epiFOXM1 KO mice | Conditional knockout | Specifically in lung epithelial cells | Reduced the number (5-fold) and size of lung tumors prior to or even after tumor initiation | |
SP-C–rtTAtg/− / tetOFOXM1-ΔNtg/− mice termed epiFOXM1-ΔN mice | Activated FOXM1-ΔN mutant | Epithelial cells | Enhanced radiation-induced pulmonary fibrosis | [9] |
SPC-rtTA/TetO-KrasG12D | Mutant KrasG12Dtranscript | Respiratory epithelial cells | Activated Kras alone is sufficient to induce formation of lung adenocarcinomas | [24] |
SPC-rtTA/TetO-GFP-FOXM1-ΔN/TetO-Kras mice, termed epFOXM1/ep Kras | Activated FOXM1-ΔN mutant and Kras | Respiratory epithelial cells | Tumor sizes are larger than those in epKras mice; FOXM1-ΔN cooperates with activated Kras to accelerate lung tumor growth | [16] |
epKrasG12D/epFOXM1−/− mice | Mutant KrasG12D transcript but deletion of FOXM1 | Lung epithelial cells | Prevented the initiation of lung tumors; reduced the number and size of lung tumors; single lung tumors were positive for FOXM1 | [24] |
Tie2-Cre/FOXM1fl/fl mice termed enFOXM1−/− mice | Deletion | Endothelial cells | Increased lung inflammation and activation of canonical Wnt signaling; increased the lung tumor number and size | [46] |
CCSP-rtTA/ TetO-GFP-FOXM1-ΔN mice, termed CCSP-FOXM1 mice | Activated FOXM1-ΔN mutant | Clara cells | Induced airway hyperplasia at sites expressing the transgene | [16] |
CCSP-FOXM1−/− mice | Conditional deletion | Clara cells | Reduced pulmonary inflammation and decreased airway resistance after HDM challenge | [67] |
FOXM1fl/fl Col1a2-Cre-ER (T)+/0 mice | Selective deletion | Activated fibroblasts | Reduced alveolar infiltration and collagen deposition; attenuated bleomycin-induced pulmonary fibrosis even during the fibrotic phase | [91] |
sm-FOXM1+/− mice | Constitutive knockdown | Smooth muscle cells | Inhibited hypoxia-induced PH and reversed existing vessel remodeling in hypoxic mice | [96] |
sm-FOXM1−/− mice | Knockout | Smooth muscle cells | Induced embryonic lethality in mice | [96] |
LysM-Cre/FOXM−/−mice | Deletion | Myeloid-derived inflammatory cells | Reduced pulmonary inflammation and airway resistance after HDM challenge | [65] |