Bo Sun1, Juan Hua2, Hongwei Cui1, Hongfeng Liu1, Kang Zhang1, Haiyan Zhou3. 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.
OBJECTIVES: In this study, we assessed the expression and functional mechanism of microRNA-1197 (miR-1197) in humannon-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 humantumors. 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.
Authors: James Saller; Kun Jiang; Yin Xiong; Sean J Yoder; Kevin Neill; Jose M Pimiento; Luis Pena; F Scott Corbett; Anthony Magliocco; Domenico Coppola Journal: Dig Dis Sci Date: 2021-03-13 Impact factor: 3.199