Wenting Geng1, Mengru Qiu2, Dongbin Zhang3, Peng Li2, Gangyi Sun3, Xi Zhou2. 1. The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong First Medical University & Shandong Academy of Medical Sciences Jinan 250102, Shandong, China. 2. Occupational Diseases Hospital of Shandong First Medical University & Shandong Province Hospital of Occupational Diseases Jinan 250002, Shandong, China. 3. Affiliated Hospital of Shandong University of Traditional Chinese Medicine Jinan 250011, Shandong, China.
Abstract
OBJECTIVE: Lung cancer remains one of the common cancers worldwide. Both LncRNA PCAT7 and miR-486-5p are tightly correlated with NSCLC. However, the relationship between PCAT7 and miR-486-5p and the detailed mechanisms underlying the effect of PCAT7 on NSCLC are not discovered yet. METHODS: GEPIA and ENCORI databases were used to determine the expression of PCAT7 in different cancers. CCK8, colony formation and Transwell assay were used to confirm the ability of cells. Luciferase reporter gene assay was employed to estimate the luciferase activity of the gene. Flow cytometry was used to compare cell cycle of NSCLC cells after indicated treatment. RESULTS: GEPIA combined ENCORI database illustrated that LncRNA PCAT7 was upregulated dramatically in NSCLC. The mRNA level of PCAT7 cells was higher than that in normal cells. Silencing PCAT7 inhibited the progression of NSCLC cells significantly. Data from ENCORI website showed that miR-486-5p was the target of PCAT7 and was negatively controlled by it. The data also showed that CDK4 could be bound and negatively regulated by miR-486-5p. MiR-486-5p inhibitor or CDK4 could partly restore the inhibitory effect of PCAT7 in NSCLC cells. In addition, silencing PCAT7 could arrest cell cycle to S in addition to G2 stage while transfecting miR-486-5p inhibitor or CDK4 could partially eliminate the retarding effects. CONCLUSION: In our study, we elaborated that LncRNA PCAT7 could promote the development of NSCLC cells by accelerating cell cycle via miR-486-5p/CDK4 axis. AJTR
OBJECTIVE: Lung cancer remains one of the common cancers worldwide. Both LncRNA PCAT7 and miR-486-5p are tightly correlated with NSCLC. However, the relationship between PCAT7 and miR-486-5p and the detailed mechanisms underlying the effect of PCAT7 on NSCLC are not discovered yet. METHODS: GEPIA and ENCORI databases were used to determine the expression of PCAT7 in different cancers. CCK8, colony formation and Transwell assay were used to confirm the ability of cells. Luciferase reporter gene assay was employed to estimate the luciferase activity of the gene. Flow cytometry was used to compare cell cycle of NSCLC cells after indicated treatment. RESULTS: GEPIA combined ENCORI database illustrated that LncRNA PCAT7 was upregulated dramatically in NSCLC. The mRNA level of PCAT7 cells was higher than that in normal cells. Silencing PCAT7 inhibited the progression of NSCLC cells significantly. Data from ENCORI website showed that miR-486-5p was the target of PCAT7 and was negatively controlled by it. The data also showed that CDK4 could be bound and negatively regulated by miR-486-5p. MiR-486-5p inhibitor or CDK4 could partly restore the inhibitory effect of PCAT7 in NSCLC cells. In addition, silencing PCAT7 could arrest cell cycle to S in addition to G2 stage while transfecting miR-486-5p inhibitor or CDK4 could partially eliminate the retarding effects. CONCLUSION: In our study, we elaborated that LncRNA PCAT7 could promote the development of NSCLC cells by accelerating cell cycle via miR-486-5p/CDK4 axis. AJTR