Figures & data
Figure 1. Lidocaine inhibited the growth of lung cancer cells. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Cell viability, (B) apoptosis rate, and (C–E) expression of apoptosis-related proteins were measured using CCK-8 assay, flow cytometry and western blot. * indicates p < .05 vs. control (Ctrl) group.
![Figure 1. Lidocaine inhibited the growth of lung cancer cells. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Cell viability, (B) apoptosis rate, and (C–E) expression of apoptosis-related proteins were measured using CCK-8 assay, flow cytometry and western blot. * indicates p < .05 vs. control (Ctrl) group.](/cms/asset/a79dcd3d-ba3a-4571-adac-064a695077d6/ianb_a_1636807_f0001_b.jpg)
Figure 2. Lidocaine inhibited the metastasis of lung cancer cells. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Migration, (B) invasion, and (C,D) expression of metastasis-related proteins were measured using Transwell assay and western blot. * indicates p < .05 vs. control (Ctrl) group.
![Figure 2. Lidocaine inhibited the metastasis of lung cancer cells. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Migration, (B) invasion, and (C,D) expression of metastasis-related proteins were measured using Transwell assay and western blot. * indicates p < .05 vs. control (Ctrl) group.](/cms/asset/0498f962-a62d-42ff-942b-7b490248d9b7/ianb_a_1636807_f0002_c.jpg)
Figure 3. Lidocaine up-regulated the expression of miR-539. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The expression of miR-539 was tested using qRT-PCR. *indicates p < .05 vs. control (Ctrl) group.
![Figure 3. Lidocaine up-regulated the expression of miR-539. A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The expression of miR-539 was tested using qRT-PCR. *indicates p < .05 vs. control (Ctrl) group.](/cms/asset/f552f012-156f-4dd6-8667-e4b7c0c28f32/ianb_a_1636807_f0003_b.jpg)
Figure 4. Lidocaine inhibited the growth of lung cancer cells via up-regulating miR-539. (A) A549 and NCI-H1299 cells were transfected with miR-539 inhibitor or NC. The expression of miR-539 was tested using qRT-PCR. The transfected cells were treated by 8 mM lidocaine for 24 h. (B) Cell viability, (C) apoptosis rate, and (D–F) expression of apoptosis-related proteins were measured using CCK-8 assay, flow cytometry and western blot. * indicates p < .05 vs. control (Ctrl) or NC group. # indicates p < .05 vs. Lido + NC group.
![Figure 4. Lidocaine inhibited the growth of lung cancer cells via up-regulating miR-539. (A) A549 and NCI-H1299 cells were transfected with miR-539 inhibitor or NC. The expression of miR-539 was tested using qRT-PCR. The transfected cells were treated by 8 mM lidocaine for 24 h. (B) Cell viability, (C) apoptosis rate, and (D–F) expression of apoptosis-related proteins were measured using CCK-8 assay, flow cytometry and western blot. * indicates p < .05 vs. control (Ctrl) or NC group. # indicates p < .05 vs. Lido + NC group.](/cms/asset/c94887ca-c423-48d0-aa43-d39d891e89c7/ianb_a_1636807_f0004_b.jpg)
Figure 5. Lidocaine inhibited the metastasis of lung cancer cells via up-regulating miR-539. The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Migration, (B) invasion, and (C,D) expression of metastasis-related proteins were measured using Transwell assay and western blot. * indicates p < .05 vs. control (Ctrl) group. # indicates p < .05 vs. Lido + NC group.
![Figure 5. Lidocaine inhibited the metastasis of lung cancer cells via up-regulating miR-539. The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. (A) Migration, (B) invasion, and (C,D) expression of metastasis-related proteins were measured using Transwell assay and western blot. * indicates p < .05 vs. control (Ctrl) group. # indicates p < .05 vs. Lido + NC group.](/cms/asset/45b8fe8c-947c-4fbc-8418-ee32e1f03436/ianb_a_1636807_f0005_c.jpg)
Figure 6. EGFR was a target of miR-539. (A,B) The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The expression of EGFR protein was tested using western blot. (C) The predicted binding sites between miR-539 and the 3’UTR of EGFR. (D) Luciferase activity assay was utilized to confirm the binding effects between miR-539 and EGFR. * indicates p < .05 vs. control (Ctrl) or NC group. # indicates p < .05 vs. Lido + NC group.
![Figure 6. EGFR was a target of miR-539. (A,B) The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The expression of EGFR protein was tested using western blot. (C) The predicted binding sites between miR-539 and the 3’UTR of EGFR. (D) Luciferase activity assay was utilized to confirm the binding effects between miR-539 and EGFR. * indicates p < .05 vs. control (Ctrl) or NC group. # indicates p < .05 vs. Lido + NC group.](/cms/asset/9ccc14b9-04f6-4c23-bac3-d2b6aa72b7d7/ianb_a_1636807_f0006_b.jpg)
Figure 7. Lidocaine suppressed the activation of ERK and PI3K/AKT pathways via up-regulating miR-539. The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The phosphorylation levels of (A,B) ERK, (C,D) PI3K and AKT were determined using western blot. * indicates p < .05 vs. control (Ctrl) group. # indicates p < .05 vs. Lido + NC group.
![Figure 7. Lidocaine suppressed the activation of ERK and PI3K/AKT pathways via up-regulating miR-539. The transfected A549 and NCI-H1299 cells were treated by 8 mM lidocaine for 24 h. The phosphorylation levels of (A,B) ERK, (C,D) PI3K and AKT were determined using western blot. * indicates p < .05 vs. control (Ctrl) group. # indicates p < .05 vs. Lido + NC group.](/cms/asset/88ed61af-be1d-4952-95cf-cc9c47f798c8/ianb_a_1636807_f0007_b.jpg)
Availability of data and materials
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.