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.

Low Smad3 is associated with lung cancer.

Zyxin is a transforming growth factor-beta (TGF-beta)/Smad3 target gene that regulates lung cancer cell motility via integrin alpha5beta1.

SMAD2 and SMAD3 acetylatation by P300-CBP is mediated by TGFB1 in human lung cancer cells.

Using a human CTL system model based on a CD8(+)/CD103(-) T cell clone specific of a lung tumor-associated Ag, we demonstrated that the transcription factors Smad2/3 and NFAT-1 are two critical regulators of this process.

Together, our findings defined an essential role for the KMT1E/SMAD2/3 repressor complex in TGFbeta-mediated lung cancer metastasis.

our findings suggest that Ski represses TGF-b-induced EMT and invasion by inhibiting SMAD-dependent signaling in non-small cell lung cancer.Ski-silenced and overexpressed A549 cells showed an increase and a reduction in the SMAD3 phosphorylation level

HoxB7 is associated with tumor metastasis in patients with lung adenocarcinoma and HoxB7 may be implicated in promoting the development of lung adenocarcinoma through activation of the TGF-beta/SMAD3 signaling.

High SMAD3 expression is associated with increased lung adenocarcinoma.

miR-206 and miR-140, as tumor suppressors, induced lung adenocarcinoma cell death and inhibited cell proliferation by modifying oncogenic TRIB2 promoter activity through p-Smad3.

SMAD3 promotes the progression of non-small cell lung cancer by up-regulating PAX6 expression.

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 .

HCP5 is a SMAD3-responsive long non-coding RNA that promotes lung adenocarcinoma metastasis via miR-203/SNAI axis.

MicroRNA-140's inhibition on the cell migration and invasion of non-small cell lung cancer by down-regulating Smad3 expression.

Mechanism of epithelialmesenchymal transition inhibited by miR203 in nonsmall cell lung cancer.

MYOCD and SMAD3/SMAD4 form a positive feedback loop and drive TGF-beta-induced epithelial-mesenchymal transition in non-small cell lung cancer.

PDLIM5 inhibits STUB1-mediated degradation of SMAD3 and promotes the migration and invasion of lung cancer cells.