| Objective To observe the regulation of proliferation and apoptosis of non-small cell lung cancer（NSCLC） cells by long chain non-coding RNA 662（LINC00662） and explore its potential mechanism of action. Methods Cancer tissue and adjacent tissue samples（≥3 cm away from the lesion） were collected from 35 NSCLC patients admitted to Zhongwu Hospital of Suqian City from March 2019 to January 2022. Normal human lung epithelial cells BEAS-2B and NSCLC cell lines A549, HCC827 and NCI-H1299 were cultured in vitro, and the expression of LINC00662 and miR-16-5p in NSCLC cancer tissues and cell lines was detected by RT-qPCR. A549 cells were transfected and grouped: si-NC group（transfected with si-NC）, si-LINC00662 group（transfected with si-LINC00662）, miR-NC group（transfected with miRNC）, amiR-16-5p group（transfected with miR-16-5p mimic）, anti-miR-NC group（transfected with anti-miR-NC）, anti-miR-16-5p group（transfected with anti-miR-16-5p）, si-LINC00662+anti-miR-NC group（co-transfected with si-LINC00662 and anti-miR-NC）, siLINC00662+anti-miR-16-5p group（co-transfected with si-LINC00662 and anti-miR-16-5p）. The inhibition rate of cell proliferation was detected by a cell counting kit（CCK8）. The apoptosis was detected bu Annexin V/FITC-PI double staining assay. The targeting binding relationship between LINC00662 and miR-16-5p was verified in dual luciferase gene reporting experiment. The relationship between the expression of LINC00662 and miR-16-5p in cancer tissues was analyzed by Pearson analysis. Results Compared with adjacent tissues, the expression of LINC00662 in cancer tissues significantly increased, and the expression of miR-16-5p markedly decreased（P＜0.05）. Compared with BEAS-2B cells, the expression of LINC00662 in A549, HCC827 and NCI-H1299 cells significantly increased, and the expression of miR-16-5p markedly decreased（P＜0.05）, and the changes in A549 cells were more significant, so it was selected for follow-up experiments. Compared with the si-NC group, the inhibition rate of cell proliferation and apoptosis rate of si-LINC00662 group significantly increased（P＜0.05）. Compared with miR-NC group, the inhibition rate of proliferation and apoptosis rate of miR-16-5p group significantly increased（P＜0.05）. Compared with si-LINC00662+anti-miR-NC group, the inhibition rate of cell proliferation and apoptosis rate in si-LINC00662+anti-miR-16-5p group significantly decreased（P＜0.05）. Compared with the si-NC group, the expression of miR-16-5p in si-LINC00662 group significantly increased（P＜0.05）. The results of double luciferase gene report experiment showed that LINC00662 could target miR-16-5p and reduce luciferase activity. Pearson analysis showed that the expression of LINC00662 in cancer tissues was negatively correlated with the expression of miR-16-5p（r=-0.364, P＜0.05）. Conclusion LINC00662 is highly expressed in NSCLC, promoting cancer cell proliferation and inhibiting apoptosis, and its potential mechanism is related to the targeted binding of miR-16-5p. |
