Aberrant ligand-dependent SHH signaling activation occurs frequently in non-small cell lung carcinomas.

While autonomous Gli activity controls non-small cell lung cancer (NSCLC) proliferation, increased Shh expression by NSCLC is associated with fibroblast activation in tumor-associated stroma.

Low expression of Sonic hedgehog signaling proteins is related to lepidic predominant subtype in primary lung adenocarcinoma.

High SHH expression is associated with lymph node metastasis in non-small cell lung cancers.

High Shh expression is associated with visceral pleural invasion and lymphatic thromboembolism in non-small-cell lung cancer.

The sonic hedgehog protein, through its receptors, plays a role in embryo development, in idiopathic pulmonary fibrosis, and in small cell lung carcinoma, non-small cell lung carcinoma and malignant pleural mesothelioma. Review.

High SHH expression is associated with Small Cell lung cancer.

Differential expression of sonic hedgehog in lung adenocarcinoma and lung squamous cell carcinoma

Dysregulated Kras/YY1/ZNF322A/Shh transcriptional axis enhances neo-angiogenesis to promote lung cancer progression.

Downregulation of miR-506-3p Facilitates EGFR-TKI Resistance through Induction of Sonic Hedgehog Signaling in Non-Small-Cell lung cancer Cell Lines.

Stromal Hedgehog pathway activation by IHH suppresses lung adenocarcinoma growth and metastasis by limiting reactive oxygen species.