MicroRNA-1197 downregulation inhibits proliferation and migration in human non- small cell lung cancer cells by upregulating HOXC11 - 31/07/19
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Graphical abstract |
Highlights |
• | MiR-1197 is upregulated in both NSCLC cancer cell lines and human tumors. |
• | MiR-1197 inhibition suppressed NSCLC in vitro and in vivo functions. |
• | HOXC11 was closely and inversely correlated with miR-1197 in NSCLC. |
• | HOXC11 inhibition augmented cancer functions in miR-1197-downregulated NSCLC cells. |
Abstract |
Objectives |
In this study, we assessed the expression and functional mechanism of microRNA-1197 (miR-1197) in human non-small cell lung cancer (NSCLC).
Methods |
In both NSCLC cell lines and NSCLC human tumors, qRT-PCR was used to assess miR-1197 expression. Through lentiviral transduction, miR-1197 was downregulated in two NSCLC cell lines, H510A and A549 cells. The functional regulations of miR-1197 downregulation on cancer cellin vitro proliferation and migration, as well as in vivo development, were assessed by MTT, transwell and xenograft assays, respectively. The association of miR-1197 on its putative downstream target gene, Homeobox C11 (HOXC11), was assessed by dual-luciferase reporter assay and qRT-PCR, respectively. Finally, HOXC11 was further inhibited in miR-1197-downregulated H510A and A549 cells to assess its mechanistic correlation with miR-1197 in regulating NSCLC in vitro proliferation and migration.
Results |
MiR-1197 was discovered to be predominantly upregulated in both NSCLC cancer cell lines and human tumors. MiR-1197 inhibition was able to suppress NSCLCin vitro proliferation and migration, as well as in vivo xenograft development. Biochemical analysis revealed that HOXC11 inversely regulated with miR-1197 in NSCLC. In double infected H510A and A549 cells, whose HOXC11 expression was further inhibited after miR-1197 downregulation, in vitro proliferation and migration were significantly augmented.
Conclusion |
MiR-1197 was upregulated in NSCLC and its downregulation has tumor-suppressing effects in NSCLC, very likely through inverse regulation on downstream target gene of HOXC11.
Le texte complet de cet article est disponible en PDF.Keywords : NSCLC, miR-1197, HOXC11, Proliferation, Migration
Plan
Vol 117
Article 109041- septembre 2019 Retour au numéro
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