the current study provides, for the first time, an important link between let-7c-mediated tumor growth inhibition, G1-phase cell cycle arrest of non-small cell lung cancer cells and the downregulation of HOXA1/CCND1, CDC25A and CDK2.

This study suggests an important role for let-7c in the molecular etiology of chemoresistant lung adenocarcinoma.

ITGB3 and MAP4K3 are directly repressed by let-7c, altering the metastatic potential of lung cancer cells.

CCAT1 is upregulated in docetaxel-resistant lung adenocarcinoma cells; its oncogenic function depends on sponging of let-7c, which releases Bcl-xl, promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes

Low Let-7C expression is associated with lung cancer.

Hsa-let-7c exerts an anti-tumor function by negatively regulating ANP32E in lung adenocarcinoma.