Activation of peroxisome proliferator-activated receptor-gamma stimulates the growth arrest and DNA-damage inducible 153 gene in non-small cell lung carcinoma cells.

PPARgamma ligands inhibit human lung carcinoma cell growth and induce apoptosis by stimulating the cyclin-dependent kinase inhibitor p21.

PPAR-gamma has a role in inhibiting angiogenesis in non-small cell lung cancer

ERK5-dependent activation of PPARgamma represents a major effector pathway mediating the anti-tumorigenic effects of Wnt 7a and Fzd 9 in non-small cell lung cancer cells

hPPAR gamma1(tr) is expressed strongly in tumorous tissues of primary human lung SCC and its overexpression renders transfected cells more resistant to chemotherapeutic drug- and chemical-induced cell death.

Apoptotic action of PPARG activation in non-small-cell lung carcinoma is mediated via proline oxidase-induced ROS formation.

PPAR-gamma polymorphisms and their interaction with smoking may contribute to the etiology of lung cancer

In many tumor cells, including lung carcinoma cells, activation of PPARgamma results in decreased cellular proliferation

analysis of a novel sequence-specific synergy between PPAR-gamma ligands and chemotherapeutic agents for lung cancer treatment

PPARgamma is activated in cigarette smoking-related lung cancer

The activity of the Sprouty4 promoter is increased by Wnt7A/Frizzled 9 homolog (Fzd9) signaling through peroxisome proliferator-activated receptor gamma in lung cancer cells.

Activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma) inhibits transforming growth factor beta (TGF-beta)-induced epithelial-mesenchymal transition in lung cancer cells and prevents metastasis by antagonizing Smad3 function.

Evaluated clinical significance of PPAR-gamma in NSCLC. Positive PPAR-gamma expression was prominent in 45 % out of 67 NSCLC cases. PPAR-gamma positivity was more frequently observed in squamous cell lung carcinoma cases compared to lung adenocarcinoma ones.

Suppression of KEAP1 in lung tumor cells resulted in increased expression of PPARgamma and was accompanied by induction of cell differentiation markers andattenuated expression of cancer stem cell markers.

These results indicate the reciprocal relationship between NR0B1 and PPARgamma on the malignant grade of lung adenocarcinoma

Data suggest that MMP2 expression in lung neoplasms can be regulated by dietary factors; here, metabolites of quercetin (an antioxidant, anticarcinogenic dietary supplement) quercetin-3-glucuronide and quercetin 3'-sulfate down-regulates expression of MMP2 in A549 cells; the mechanism for this enzyme repression appears to involve up-regulation of PPARgamma.

UCP2 is a key mediator of hypoxia-triggered chemoresistance in non-small cell lung cancer cells via repression of peroxisome proliferator-activated receptor gamma.

ALDH1A3 suppression could be one of PPARG tumor suppressive function. This study provides a better understanding of the role of PPARG in lung cancer.

Data indicate that PPAR-g agonists represent an attractive treatment tool and by suppression of cell growth (in vitro and ex vivo models) and of invasion via blockade of MAPK cascade and TGFb/SMADs signaling, respectively, and its role in cancer bioenergetics and metabolism indicate that PPAR-g agonists represent an attractive treatment tool for non small cell lung cancer .

The influence of conjugated linoleic acid on the expression of peroxisome proliferator-activated receptor-gamma and selected apoptotic genes in non-small cell lung cancer.

PPARgamma is a critical target for prostacyclin-mediated lung cancer chemoprevention and may also have therapeutic activity.

The reduction of endogenous PPARgamma ligands and increased PPARalpha occurred before the formation of lung tumors, indicating that the molecular changes play a role in lung carcinogenesis.

Activation of PPARgamma in myeloid cells promotes lung cancer progression and metastasis.

Low expression of PPARG is associated with squamous cell lung carcinoma.

Activation of PPARgamma in Myeloid Cells Promotes Progression of Epithelial lung tumors through TGFB1.