MiR-760 inhibits lung cancer cells through mitogen-activated protein kinase signaling pathway

Abstract

Our study assesses miR-760’s role in the proliferation, invasion and migration of non-small cell lung cancer (NSCLC) cells. Lung cancer A549 cells were assigned into BL group (no transfection), ZN group (transfection of NC), and ZM group (transfection of miR-760 mimics). The miR-760 level, cell viability, apoptosis, invasion, migration ability, ERK1, JNK, and p38MAPK protein expression were analyzed using Real Time Quantitative polymerase chain reaction (RT-qPCR), MTT, Hoechst33258 fluorescence staining, Transwell cell, cell scratch test, and Western blot. Compared with other groups, miR-760 expression in ZM group was the highest, indicating a successful transfection (P <0.05). 48, 72, and 96 hours later, A549 cell viability in ZM group was the lowest with a significant difference from other groups (P <0.05). The cell viability reached a peak after 96 hours of culture (P <0.05) with higher cell viability of BL group than ZN group (P >0.05). A549 cells in ZM group showed significantly higher cell apoptosis rate and lower cell invasion rate than ZN and BL group (P <0.05). The number of cell invasion (220.71±15.37) and migration in BL group (220.37±17.60) is similar to ZN group (215.32±15.62 and 217.26±15.94) (P >0.05). In addition, cell migration number in ZM group (99.62±12.01) was less than ZN and BL group (P <0.05). ERK1, JNK and p38MAPK protein expression in ZM group was the lowest (P <0.05) and those in BL group was close to ZN group (P >0.05). Upregulating miR-760 in A549 cancer cells can inhibit cell proliferation via regulation of MAPK signaling pathway.