LncRNA GAS5 inhibits Invasion and Migration of Lung Cancer through influencing EMT process

• Published in: Journal of Cancer Vol. 12; no. 11; pp. 3291 - 3298
• Main Authors: Zhu, Lihuan, Zhou, Dongsheng, Guo, Tianxing, Chen, Wenshu, Ding, Yun, Li, Wujing, Huang, Yangyun, Huang, Jianyuan, Pan, Xiaojie
• Format: Journal Article
• Language: English
• Published: Australia Ivyspring International Publisher Pty Ltd 01.01.2021; Ivyspring International Publisher
• Subjects: Antibodies; Bladder cancer; Cell adhesion & migration; Cell growth; Chemotherapy; Experiments; Flow cytometry; Gene expression; Kidney cancer; Laboratory animals; Lung cancer; Metastasis; Research Paper; Tumors; Variance analysis; Beijing China; China; lung cancer; E-cadherin; EMT; GAS5
• ISSN: 1837-9664; 1837-9664
• DOI: 10.7150/jca.56218

Lung cancer is a malignant tumor in mammary gland epithelium with high morbidity and mortality among women worldwide. Long noncoding RNA GAS5 (GAS5) has been proved to be closely related with tumor progression. However, the influence of GAS5 on lung cancer and the specific mechanism remain unclear. Cell invasion, cell migration, cell apoptosis and cell cycle were investigated after transfection with pcDNA-GAS5 and sh-GAS5. Sizes of tumors were measured by establishing transplanted tumor model . E-cadherin and N-cadherin expressions were investigated. Cell invasion and migration were inhibited markedly in GAS5 overexpressed cell line. Cell cycle results indicated that the percentage of S-phase cells was increased, and G2-phase was reduced in the GAS5 overexpression cell line. Tumor size was suppressed obviously after GAS5 overexpression treatment. GAS5 markedly inhibited the expression of E-cadherin and induced the expression of N-cadherin. GAS5 overexpression significantly inhibited lung cancer cell proliferation by increasing the E-cadherin and decreasing N-cadherin. These findings provide novel evidence that GAS5 can be viewed as an anti-lung cancer agent through affecting EMT pathway.