MiR-21/Sonic Hedgehog (SHH)/PI3K/AKT Pathway is Associated with NSCLC of Primary EGFR-TKI Resistance

Background: Non-small cell lung cancer (NSCLC), caused by abnormal gene drive, may have primary drug resistance after treatment with tyrosine kinase inhibitors (EGFR-TKIs). Therefore, we explore whether the drug-resistant NSCLC treated EGFR-TKI is related to miR-21/Sonic Hedgehog (SHH)/PI3K/AKT pathway. Methods: The patients from our hospital who meet AJCC TNM staging (7th edition) stage IIIB and IV were selected in this case study. Thereafter, response of EGFR-TKIs was evaluated according solid tumor efficacy evaluation standard (version 1.1). divided into group (EGFR-TKIs-Primary-R) sensitive (EGFR-TKIs-Primary-S). Apoptosis level degree fibrosis patients’ tissues detected TUNEL assay Masson staining, respectively. levels miR-21 GLI1 measured qRT-PCR technique. contents E-cadherin Snail IF method, PI3K/AKT phosphorylation using IHC Results: Compared EGFR-TKIs-Primary-S group, EGFR-TKIs-Primary-R showed lower apoptosis tissue fibrosis. miR-21, GLI1, Snail, p-PI3K p-AKT increased, while decreased. However, total protein PI3K AKT remained same. Conclusion: found be miR-21/SHH, process epithelial mesenchymal transition (EMT), phosphorylation. present study provides a reference for future research resistance, paves way discover new therapeutic targets alleviate resistance.