The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers.

Snail upregulation plays a role in non-small cell lung carcinoma by promoting tumor progression mediated by CXCR2 ligands

nuclear expression parallels higher malignancy in neuroendocrine lung tumors

novel evidence that inhibition of BMP-2 or BMP-2-mediated MAPK/Runx2/Snail signaling is an attractive therapeutic target for osteolytic bone metastases in lung cancer patients.

The functional germline variant c.353T>C (p.Val118Ala) of Snai1 confers consistently decreased risks of lung cancer and COPD, and this variant affects lung cancer risk through a mediation effect of COPD.

Snail1 may be a co-factor of TERT enhancer rs2853677 for predicting lung adenocarcinoma susceptibility and prognosis

Data suggest that silencing Snail decreases the malignant behaviors of lung cancer cells by reversing epithelial-to-mesenchymal transition processes and causing cell cycle defects.

E-cadherin expression was increased by transfection of p300 small interfering RNA in a dose-dependent manner.. There was a correlation between Snail and p300 expressions in lung cancer. Moreover, p300 acetylates Snail both in vivo and in vitro, and K187 may be involved in this modification.

MiR-22 over-expression attenuated lung cancer cell EMT and invasion via targeted inhibiting Snail.

Neutrophils and Snail orchestrate the establishment of a pro-tumor microenvironment in lung cancer.

-box and WD repeat domain containing 7 (FBW7) silencing stabilized Snail protein and induced epithelial-to mesenchymal transition (EMT), and acquisition of migration and invasion properties in non-small cell lung cancer (NSCLC).

study defines a Snail-ESRP1 cancer axis that is crucial for human lung carcinogenesis, with implications for new intervention strategies and translational opportunities

Study provide evidence that Snail plays a key role in DLL3-mediated small cell lung cancer-cell migration and invasion.

SNAI1 levels in exosomes secreted from cancer-associated fibroblasts (CAFs) were correlated with SNAI1 expression in CAFs. Furthermore, the level of SNAI1 in exosomes was crucial for inducing Epithelial-mesenchymal transition in lung cancer cells.

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

findings reveal a tumour-suppressive role of UDP-glucose in lung cancer metastasis and uncover a mechanism by which UDP-glucose 6-dehydrogenase (UGDH) promotes tumour metastasis by increasing the stability of SNAI1 mRNA

Relevance and prognostic ability of Twist, Slug and tumor spread through air spaces in lung adenocarcinoma.