Loss of Smad4 expression is associated with lymph node metastasis in lung adenocarcinoma

Studies establish Smad4 as a lung tumor suppressor and suggest that the defective DNA repair phenotype of Smad4-deficient tumors can be exploited by specific therapeutic strategies.

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

AhR affects the transforming growth factor-beta signaling pathway by inducing Smad4 degradation by the proteasome and suppressing tumor metastasis via epithelial to mesenchymal transition reduction in lung cancer cells.

lung metastases from colorectal cancer patients revealed that CCL15 expression correlated with loss of SMAD4. In a mouse model, CCL15 secreted from SMAD4-deficient colorectal cancer cells recruited CCR1(+) cells, promoting their metastatic activities to the lung.

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.

reduced Smad4 expression may predict responsiveness to regimens that contain DNA topoisomerase inhibitors in human non-small cell lung cancer

our data suggest that miR-1285-5p functions as a tumor promoter in the development of non-small-cell lung carcinoma by targeting Smad4 and CDH1, indicating a novel therapeutic strategy for non-small-cell lung carcinoma patients.

current study revealed that low FSTL1, BMP4, and Smad4 expression significantly predict poor prognosis in lung adenocarcinoma but not in squamous cell carcinoma.

The role of SMAD4 signaling in the lung squamous cell carcinoma.

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

PARP-1 induces EMT in non-small cell lung carcinoma cells via modulating the transcription factors Smad4, p65 and ZEB1.