Abstract
BackgroundLncRNA PLAC2 has been characterized as a tumor suppressive lncRNA in glioma. We investigated the role of PLAC2 in non-small cell lung cancer (NSCLC).MethodsA total of 187 NSCLC patients were admitted by The First Hospital of Jilin University from December 2010 to December 2014. All the patients were diagnosed by histopathological approaches. Transient cell transfections, RT-qPCR, invasion, and migration ability measurement, were applied for the experiments.ResultsPLAC2 was down-regulated, while miR-21 was up-regulated in NSCLC tissues compared to non-cancer tissues. Low PLAC2 levels in NSCLC tissues were associated with poor survival of NSCLC patients. PLAC2 and miR-21 were inversely correlated, and PLAC 2 over-expression in NSCLC cells resulted in the down-regulation of miR-21. However, miR-21 over-expression did not significantly affect PLAC2 expression. In addition, PLAC2 over-expression resulted in decreased migration and invasion rates of NSCLC cells. MiR-21 over-expression played the opposite role and attenuated the effects of PLAC2 over-expression.ConclusionsIn conclusion, lncRNA PLAC2 down-regulated miR-21 in NSCLC and inhibited cancer cell migration and invasion.
Highlights
LncRNA PLAC2 has been characterized as a tumor suppressive Long non-coding RNAs (lncRNAs) in glioma
Expression patterns of PLAC2 and miR-21 were opposite in non-small cell lung cancer (NSCLC) PLAC2 and miR-21 in two types of tissues were detected by performing RT-qPCR, and expression data were analyzed by performed paired t-test
It was observed that compared to the levels in non-tumor tissues, PLAC2 levels were significantly lower (Fig. 1a, p < 0.05) and expression levels of miR-21 were significantly higher patients with low PLAC2 levels in NSCLC tissues had (Fig. 1a, p < 0.05) in NSCLC tissues
Summary
LncRNA PLAC2 has been characterized as a tumor suppressive lncRNA in glioma. We investigated the role of PLAC2 in non-small cell lung cancer (NSCLC). Non-small cell lung cancer (NSCLC) is the major subtype of lung cancer, with a high prevalence and mortality rate [1]. Metastasis of neoplasms, which occurs in most NSCLC patients, is the major cause of cancerrelated death [2, 3]. The overall 5-year survival rate of these patients is quite low [3]. Efforts have been paid to the identification of molecular mechanisms involved in the regulation of cancer cell migration and invasion [4, 5]. The pathogenesis of NSCLC is still largely unknown, which limits the development of novel therapeutic approaches to improve the survival of NSCLC patients. A small number of genetic alterations has been identified in NSCLC [6, 7], and the functions of those genes are
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