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. 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. 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.