ABSTRACT
INTRODUCTION: Tartrate-resistant acid phosphatase 5 (ACP5), which is essential for bone resorption and osteoclast differentiation, promotes cell motility through the modulation of focal adhesion kinase phosphorylation. This study seeks to elucidate the association of ACP5 expression and the clinicopathologic characteristics of patients with lung adenocarcinoma (AD). METHODS: The expression of ACP5 was measured by Immunohistochemistry and Western blot analysis in lung AD and matched tumor-adjacent tissues, and the χ2 test was applied to analyze the correlation between ACP5 expression and clinicopathologic features. Using the Kaplan-Meier method, univariate and multivariate regression analysis was to explore the correlation between ACP5 expression and overall survival (OS). RESULTS: We found that ACP5 was frequently upregulated in lung AD tissues. The high expression of ACP5 was significantly related to lymph node status, tumor-node-metastasis (TNM) stage, and differentiation. From the results of univariate survival analysis, it indicated that the patients with high expression of ACP5 expression had a significantly lower OS than the patients with low expression of ACP5 expression. As it showed in Multivariate Cox regression analysis, the high expression of ACP5 expression was an independent prognostic factor for OS. CONCLUSIONS: Our results suggest that high expression of ACP5 correlates with tumor progression and may serve as a potential prognostic biomarker in lung AD.
Subject(s)
Adenocarcinoma/genetics , Gene Expression Regulation, Neoplastic , Lung Neoplasms/genetics , Tartrate-Resistant Acid Phosphatase/genetics , Up-Regulation , Adenocarcinoma/metabolism , Adenocarcinoma/pathology , Adenocarcinoma of Lung , Adult , Aged , Aged, 80 and over , Blotting, Western , DNA, Neoplasm/genetics , Female , Humans , Immunohistochemistry , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , Male , Middle Aged , Neoplasm Staging , Prognosis , Retrospective Studies , Tartrate-Resistant Acid Phosphatase/biosynthesisABSTRACT
Circular RNAs (circRNAs) are a type of non-coding RNAs that have been identified as critical regulators in various diseases, especially in cancers. However, the expression profiles and functions of circRNAs in cervical cancer are still unclear. In present study, human circRNAs microarray were performed to screen the circRNAs expression in cervical cancer tissue. Microarray analysis revealed 45 significantly expressed circRNAs with 4 fold change. Among these up-regulated circRNAs, hsa_circ_0018289 was validated to be significantly up-regulated in 35 pairs of cervical cancer tissue compared with adjacent normal tissue and cell lines. Loss-of-function experiments revealed that, in vitro and in vivo, hsa_circ_0018289 knockdown inhibited the proliferation, migration and invasion of cervical cancer cells. Via bioinformatics prediction program and luciferase reporter assays, hsa_circ_0018289 was observed to directly bind to miR-497. Taken together, the results indicate that hsa_circ_0018289 plays important role in cervical cancer proliferation, migration and invasion, suggesting the miRNA 'sponge' of hsa_circ_0018289 and its oncogenic role on cervical cancer tumorigenesis.
ABSTRACT
Emerging evidence suggests that the long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) gene is involved in the pathogenesis of cervical cancer. However, the potential mechanism is rarely reported. Our study found that PVT1 was upregulated in cervical cancer tissue and cell lines. After transfecting PVT1 siRNA, the proliferation, migration, and invasion of cervical cancer cells were markedly decreased. miRNA expression profiles demonstrate that miR-424 was markedly downregulated in cervical cancer tissue. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay. Pearson's correlation analysis showed that PVT1 expression was negatively related to miR-424 expression in glioma cancer tissues. Finally, lowered expression of miR-424 could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines. Our results reveal a tumor-promoting role for PVT1, acting as a competing endogenous RNA (ceRNA) or a molecular sponge in negatively modulating miR-424, which might provide a novel therapeutic target for cervical cancer.
