Low miR-221 expression is associated with recurrence of non-small cell lung cancer.

Data show that showed that miR-130a, expressed at low level in lung cancer cell lines, by targeting MET was able to reduce TRAIL resistance in non-small cell lung cancer (NSCLC) cells through the c-Jun-mediated downregulation of miR-221 and miR-222.

The relative expression levels of microRNA-221 in the non-small cell lung cancer tissues were remarkably higher than that in the corresponding normal tissues. The expression level was associated with lymph node metastasis. Patients with high expression level of microRNA-221 had shorter overall survival time than those with low expression. It was a useful independent biomarker for NSCLC prognosis.

MiR-221 together with proteins MDR1 and ABCG2 was upregulated in Cisplatin-resistant A549 lung cancer cells. Anti-miR-221 inhibits proliferation and induces senescence in lung cancer cells. PTEN/Akt pathway axis was identified as a target of drug resistance induced by miR-221.

Effects of miR-221 on the apoptosis of non-small cell lung cancer cells by lncRNA HOTAIR.

Molecular experiments showed that miR2213p was able to bind with the 3'untranslated region (UTR) of p27 and decreased the expression of p27 in nonsmall cell lung cancer cells.