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Biomed Pharmacother. 2019 Jun 7;117:109041. doi: 10.1016/j.biopha.2019.109041. [Epub ahead of print]

MicroRNA-1197 downregulation inhibits proliferation and migration in human non- small cell lung cancer cells by upregulating HOXC11.

Author information

1
Department of Thoracic Surgery, Jining No.1 People's Hospital, Jining 272111, Shandong, China.
2
Lung disease division, Jining Hospital of TCM, Jining 272037, Shandong, China.
3
Health management center, Weifang People's Hospital, Weifang 261041, Shandong, China. Electronic address: zhou_haiyan@aol.com.

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.

KEYWORDS:

HOXC11; Migration; NSCLC; Proliferation; miR-1197

PMID:
31181445
DOI:
10.1016/j.biopha.2019.109041
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