Abstract 378P
Background
Epithelial-mesenchymal transition (EMT) is one of the major molecular mechanisms inducing tumor invasion and metastasis. Long non-coding RNA (LncRNA) has been reported to be involved in cancer stem cell function and EMT. However, the role of lncRNA RP11-888D10.4 in metastasis in lung cancer have not been well demonstrated in the literature.
Methods
qRT-PCR was performed to determine lncRNA RP11-888D10.4 expression in samples from patients with resected lung adenocarcinoma. Transfection and knockdownof lncRNA RP11-888D10.4 was performed in H1299 cells and A549 cells, respectively. Western blotting analysis was performed to demonstrated E-cadherin and vimentin expression. Migration assay and matrigel invasion assay were done to determine the EMT phenotypes after lncRNA RP11-888D10.4 transfection or knockdown in lung cancer cells. Tail vein assay was performed to test if lncRNA RP11-888D10.4 increases in vivo metastatic activity.
Results
High lncRNA RP11-888D10.4 expression was significantly associated with predominant pattern group (micropapillary/solid vs. lepidc/acinar/papillary) in patients with lung adenocarcinoma.Western blotting analysis showed decreased E-cadherin and increased vimentin expression in H1299 cells after lncRNA RP11-888D10.4 transfection. Western blotting analysis also showed decreased vimentin expression and increased E-cadherin expression in A549 cells after lncRNA RP11-888D10.4 knockdown. Migration assay showed that migration increased in H1299-RP11-888D10.4 cells, but decreased in A549-RP11-888D10.4i cells. Matrigel invasion assay showed the invasiveness increased in H1299-RP11-888D10.4 cells, but decreased in A549-RP11-888D10.4i cells. The mice being injected with H1299-RP11-888D10.4 cells had significantly more pulmonary nodules than did those with H1299-Mock cells sixteen weeks after injection.
Conclusions
High lncRNA RP11-888D10.4 expression was significantly associated with predominant pattern group in patients with lung adenocarcinoma. LncRNA RP11-888D10.4 expression upregulates invasion and metastasis through epithelial-mesenchymal transition in lung cancer cells.
Funding
Has not received any funding
Disclosure
All authors have declared no conflicts of interest.