[No authors listed]
Cisplatin has been widely used as a conventional treatment for patients with nonâsmall cell lung cancer (NSCLC). However, primary and acquired cisplatin resistances are frequently developed during the treatment of patients with NSCLC, leading to an increased mortality rate. Accumulating evidence demonstrated that aberrantly expressed microRNAs (miRs) are involved in the development of chemoresistance. In the present study, sensitivity of NSCLC cells to cisplatin was identified to increase following overexpression of miRâ608. Conversely, sensitivity to cisplatin was reduced following miRâ608 knockdown. Reverse transcriptionâquantitative PCR and western blotting analyses identified that TEA domain transcription factor 2 (TEAD2), a key regulator of cell stemness, was negatively regulated by miRâ608 in NSCLC cells. By repressing TEAD2, miRâ608 decreased the expression level of several target genes of the Hippoâyesâassociated protein signaling pathway. Furthermore, TEAD2 mRNA was confirmed to be targeted by miRâ608 in NSCLC cells via a dualâluciferase reporter assay. Importantly, the increased cisplatin sensitivity induced by miRâ608 overexpression was reversed by transfection of TEAD2 in NSCLC cells. The present data suggested that miRâ608 may represent a novel candidate biomarker for the evaluation of cisplatin sensitivity in patients with NSCLC.
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