We are analyzing https://link.springer.com/article/10.1186/s12943-017-0710-z.

Title:
MicroRNA-218 functions as a tumor suppressor in lung cancer by targeting IL-6/STAT3 and negatively correlates with poor prognosis | Molecular Cancer
Description:
Background Aberrant expression of microRNAs in different human cancer types has been widely reported. MiR-218 acts as a tumor suppressor in diverse human cancer types impacting regulation of multiple genes in oncogenic pathways. Here, we evaluated the expression and function of miR-218 in human lung cancer and ALDH positive lung cancer cells to understand the potential mechanisms responsible for disease pathology. Also, the association between its host genes and the target genes could be useful towards the better understanding of prognosis in clinical settings. Methods Publicly-available data from The Cancer Genome Atlas (TCGA) was mined to compare the levels of miR-218 and its host gene SLIT2/3 between lung cancer tissues and normal lung tissues. Transfection of miR-218 to investigate its function in lung cancer cells was done and in vivo effects were determined using miR-218 expressing lentiviruses. Aldefluor assay and Flow cytometry was used to quantify and enrich ALDH positive lung cancer cells. Levels of miR-218, IL-6R, JAK3 and phosphorylated STAT3 were compared in ALDH1A1 positive and ALDH1A1 negative cells. Overexpression of miR-218 in ALDH positive cells was carried to test the survival by tumorsphere culture. Finally, utilizing TCGA data we studied the association of target genes of miR-218 with the prognosis of lung cancer. Results We observed that the expression of miR-218 was significantly down-regulated in lung cancer tissues compared to normal lung tissues. Overexpression of miR-218 decreased cell proliferation, invasion, colony formation, and tumor sphere formation in vitro and repressed tumor growth in vivo. We further found that miR-218 negatively regulated IL-6 receptor and JAK3 gene expression by directly targeting the 3′-UTR of their mRNAs. In addition, the levels of both miR-218 host genes and the components of IL-6/STAT3 pathway correlated with prognosis of lung cancer patients. Conclusions MiR-218 acts as a tumor suppressor in lung cancer via IL-6/STAT3 signaling pathway regulation.
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Keywords {🔍}

cancer, cells, lung, cell, pubmed, article, google, scholar, expression, levels, stat, tumor, cas, fig, ilr, jak, data, tissues, slit, signaling, positive, proliferation, microrna, genes, aldh, transfection, human, gene, normal, egfr, patients, central, aldha, nsclc, host, growth, study, mircontrol, targeting, prognosis, overexpression, stem, liu, target, reduced, tcga, assay, invasion, pathway, mirna,

Topics {✒️}

newly-identified mir-218–mediated il-6r k-ras-dependent lung tumorigenesis il-6/jak/stat3 signaling pathway large-scale clip-seq data dual-luciferase reporter system small-cell lung carcinomas therapeutically resistant k-ras il-6/jak/stat3 pathway phosphate-buffered saline/tween-20 article download pdf small-cell lung cancer small-cell lung cancer p53-induced mouse model regulating ecop-mediated suppression vertebrate-specific intronic mirna protein-rna interaction networks il-6/stat3 pathway correlated squamous cell carcinoma human il-6r antibody large cell carcinoma cell proliferation showed cancer stem cell aldh positive cells human lung cancers stat3 signaling pathway specific aldh inhibitor privacy choices/manage cookies displays reduced resistance performed cell proliferation stem cell characterics lung cancer subtypes aldefluor assay kit luciferase reporter plasmids 555-coupled secondary antibody human lung cancer targeting jak/stat3 cancer genome atlas stem cell technologies inhibits stat3 phosphorylation cancer stem cells lung cancer disease creative commons license full access argonaute clip-seq human solid cancers cell proliferation effects reduce cell growth relative luciferase activity related host genes aldh negative cells

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         description:Aberrant expression of microRNAs in different human cancer types has been widely reported. MiR-218 acts as a tumor suppressor in diverse human cancer types impacting regulation of multiple genes in oncogenic pathways. Here, we evaluated the expression and function of miR-218 in human lung cancer and ALDH positive lung cancer cells to understand the potential mechanisms responsible for disease pathology. Also, the association between its host genes and the target genes could be useful towards the better understanding of prognosis in clinical settings. Publicly-available data from The Cancer Genome Atlas (TCGA) was mined to compare the levels of miR-218 and its host gene SLIT2/3 between lung cancer tissues and normal lung tissues. Transfection of miR-218 to investigate its function in lung cancer cells was done and in vivo effects were determined using miR-218 expressing lentiviruses. Aldefluor assay and Flow cytometry was used to quantify and enrich ALDH positive lung cancer cells. Levels of miR-218, IL-6R, JAK3 and phosphorylated STAT3 were compared in ALDH1A1 positive and ALDH1A1 negative cells. Overexpression of miR-218 in ALDH positive cells was carried to test the survival by tumorsphere culture. Finally, utilizing TCGA data we studied the association of target genes of miR-218 with the prognosis of lung cancer. We observed that the expression of miR-218 was significantly down-regulated in lung cancer tissues compared to normal lung tissues. Overexpression of miR-218 decreased cell proliferation, invasion, colony formation, and tumor sphere formation in vitro and repressed tumor growth in vivo. We further found that miR-218 negatively regulated IL-6 receptor and JAK3 gene expression by directly targeting the 3′-UTR of their mRNAs. In addition, the levels of both miR-218 host genes and the components of IL-6/STAT3 pathway correlated with prognosis of lung cancer patients. MiR-218 acts as a tumor suppressor in lung cancer via IL-6/STAT3 signaling pathway regulation.
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            Lung cancer
            STAT3
            Interleukin-6 receptor
            Cancer stem cell
            Cancer Research
            Oncology
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      description:Aberrant expression of microRNAs in different human cancer types has been widely reported. MiR-218 acts as a tumor suppressor in diverse human cancer types impacting regulation of multiple genes in oncogenic pathways. Here, we evaluated the expression and function of miR-218 in human lung cancer and ALDH positive lung cancer cells to understand the potential mechanisms responsible for disease pathology. Also, the association between its host genes and the target genes could be useful towards the better understanding of prognosis in clinical settings. Publicly-available data from The Cancer Genome Atlas (TCGA) was mined to compare the levels of miR-218 and its host gene SLIT2/3 between lung cancer tissues and normal lung tissues. Transfection of miR-218 to investigate its function in lung cancer cells was done and in vivo effects were determined using miR-218 expressing lentiviruses. Aldefluor assay and Flow cytometry was used to quantify and enrich ALDH positive lung cancer cells. Levels of miR-218, IL-6R, JAK3 and phosphorylated STAT3 were compared in ALDH1A1 positive and ALDH1A1 negative cells. Overexpression of miR-218 in ALDH positive cells was carried to test the survival by tumorsphere culture. Finally, utilizing TCGA data we studied the association of target genes of miR-218 with the prognosis of lung cancer. We observed that the expression of miR-218 was significantly down-regulated in lung cancer tissues compared to normal lung tissues. Overexpression of miR-218 decreased cell proliferation, invasion, colony formation, and tumor sphere formation in vitro and repressed tumor growth in vivo. We further found that miR-218 negatively regulated IL-6 receptor and JAK3 gene expression by directly targeting the 3′-UTR of their mRNAs. In addition, the levels of both miR-218 host genes and the components of IL-6/STAT3 pathway correlated with prognosis of lung cancer patients. MiR-218 acts as a tumor suppressor in lung cancer via IL-6/STAT3 signaling pathway regulation.
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         Lung cancer
         STAT3
         Interleukin-6 receptor
         Cancer stem cell
         Cancer Research
         Oncology
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      name:Department of Pediatrics of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, People’s Republic of China
      name:Department of Pediatrics of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, People’s Republic of China
      name:Department of Pediatrics of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, People’s Republic of China
      name:Department of Biochemistry, UT Southwestern Medical Center, Dallas, USA
      name:Department of Oncology of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China
      name:Department of Radiation Oncology, UT Southwestern Medical Center, Dallas, USA
      name:School of Biological Science and Technology, University of Jinan, Jinan, China
      name:Department of Medicine, Division of Epidemiology, Vanderbilt University, Nashville, USA
      name:Department of Radiation Oncology, UT Southwestern Medical Center, Dallas, USA
      name:Department of Pediatrics of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, People’s Republic of China

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