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.

High p-Smad2 expression in stromal fibroblasts is associated with non-small cell lung cancer.

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

MicroRNA-10a silencing reverses cisplatin resistance in the A549/cisplatin human lung cancer cell line via the transforming growth factor-beta/Smad2/STAT3/STAT5 pathway

Relationship between expression of TGF-beta1, Smad2, Smad4 and Prognosis of Patients with Resected Non-small Cell lung cancer

miR-27a contributed to cell proliferation and invasion by inhibiting TGF-beta-induced cell cycle arrest. These results suggest that miR-27a may function as an oncogene by regulating SMAD2 and SMAD4 in lung cancer.

selective inhibition of SMAD3 or CCT6A efficiently suppresses TGF-beta-mediated metastasis. Findings provide a mechanism that directs TGF-beta signaling toward its prometastatic arm and may contribute to the development of therapeutic strategies targeting TGF-beta for non-small-cell lung carcinoma.

Long noncoding RNA OSER1AS1 promotes the malignant properties of nonsmall cell lung cancer by sponging microRNA4333p and thereby increasing Smad2 expression.