Background
MicroRNAs (miRNAs) play an important role in the development and progression of lots of cancer. Non-small cell lung cancer (NSCLC) is all lung cancer except small cell lung cancer (SCLC). The most common non-small cell lung cancer types include squamous cell carcinoma, large cell carcinoma and adenocarcinoma, and some other common types. Increasing studies identified that a long non-coding RNA NKILA was negatively correlated with breast cancer metastasis while its clinical significance and potential role in non-small cell lung cancer (NSCLC) remain unclear. In the present study, we confirmed the function of lncRNA NKILA as well as the underlying mechanism in regulating the NSCLC.
Conclusion
In summary, our results confirmed that low expression of lncRNA NKILA plays a role in the deterioration of NSCLC cells and this effect depends on IL-11/STAT3 signaling.
Methods
The expression of lncRNA NKILA was detected in both Lung cancer tissues and cell line including A549 and NCI-H1299 by quantitative real-time reverse transcription. A small interfering RNA (siRNA) that targeted NKILA was transfected into cells to inhibit the expression of NKILA. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and scratch experiments were performed to analyze the migration and proliferation of NCI-H1299 which were transfected with si-NKILA. Protein levels of genes that related with G0/G1 arrest markers p16, p21, and p27 markers were measured.
Results
The expression of NKILA was significantly down regulated in lung cancer tissues when compared to matched normal tissue.