Abstract
BackgroundLINC01116 is a recently identified oncogenic lncRNA in glioma. Differential expression analysis using the public gene expression analysis tool GEPIA revealed the upregulation of LINC01116 in lung cancer. We studied the functions of LINC01116 in small cell lung cancer (SCLC).MethodsThe expression of LINC01116 in several types of cancer tissue and the paired non-tumor tissues was evaluated by GEPIA. The effects of the overexpression of LINC01116 and miR-93-5p on the expression of STAT3 were evaluated. The effects of the overexpression of LINC01116, miR-93-5p and STAT3 on SHP-77 cell behaviors were evaluated by Transwell assays.ResultsLINC01116 was highly expressed in SCLC and predicted poor survival. In SCLC tissues, the expression of LINC01116 was positively correlated with STAT3. Bioinformatics analysis revealed that miR-93-5p may target LINC01116. Overexpression of LINC01116 increased STAT3 but did not affect the expression of miR-93-5p. Transwell assay showed that LINC01116 and STAT3 increased cell invasion and migration rates. MiR-93-5p played an suppressed cell behaviors and suppressed the role of LINC01116.ConclusionTherefore, LINC01116 might upregulate STA3 by sponging miR-93-5p, thereby promoting cell invasion and migration in SCLC.
Highlights
LINC01116 is a recently identified oncogenic lncRNA in glioma
We studied the crosstalk between LINC01116, miR-93-5p and STAT3 in small cell lung cancer (SCLC)
Upregulation of LINC01116 predicted poor survival of SCLC patients The expression of LINC01116 in several types of cancer tissue and the paired non-tumor tissues was evaluated by GEPIA
Summary
LINC01116 is a recently identified oncogenic lncRNA in glioma. Differential expression analysis using the public gene expression analysis tool GEPIA revealed the upregulation of LINC01116 in lung cancer. We studied the functions of LINC01116 in small cell lung cancer (SCLC). As a type of deadly tumor, small cell lung cancer (SCLC) accounts for about 1/6 of lung cancer [1]. Patients with SCLC are usually treated with platinum in combination with etoposide and topotecan, which are the first- and second-line drugs for this disease, respectively [4]. Several other drugs, such as doxorubicin, SCLC requires the involvement of molecular factors [6, 7]. Molecular facts involved in SCLC may the targets for treatment [7] STAT3 regulates inflammation, immunity and metastasis in cancer [8, 9]. Analysis of TCGA by GEPIA (http://gepia.cancer-pku.cn/) revealed the upregulation of LINC01116 in several types of lung cancer.
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