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Numerous studies have demonstrated that microRNAs (miRNAs) play vital roles in papillary thyroid carcinoma (PTC). The aim of the present study was to examine the expression levels of miR-183 in PTC and investigate whether its potential roles involved targeting the programmed cell death 4 (PDCD4). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to examine the expression levels of miR-183 in 38 PTC specimens and 4 PTC cell lines. MTT, colony formation, wound-healing and Transwell invasion assays, and flow cytometry were conducted to explore the potential functions of miR-183 in human TPC1 papillary thyroid carcinoma cells. The dual-luciferase reporter assay was performed to validate whether PDCD4 was a direct target of miR-183. The effects of modulating miR-183 on endogenous levels of PDCD4 were subsequently confirmed via RT-qPCR and western blotting. Functional assays were used to indicate the roles of endogenous PDCD4 in TPC1. The results showed the miR-183 expression levels were significantly upregulated in PTC specimens and cell lines (P

MicroRNAs (miRNAs) are a class of highly conserved, small endogenous single-strand non-coding RNAs. They are aberrantly expressed in the circulation and tissue of patients with cancer. Therefore, it has been suggested that they may act as key regulators of carcinogenesis. The aim of the present study was to examine the expression level of miR-195-5p in human breast cancer and its potential role in carcinogenesis. The expression level of miR-195-5p was measured in 40 breast cancer specimens and adjacent normal breast tissues by quantitative polymerase chain reaction (qPCR). Next, to explore the potential function of miR-195-5p, we used MDA-MB-231 human breast cancer cells and carried out MTT, colony formation, Transwell chamber migration and cell cycle assays. The dual-luciferase reporter assay was also performed to determine putative targets of miR-195-5p, which were validated using qPCR and western blot assays. We found that miR-195-5p expression was significantly decreased in the 40 breast cancer specimens when compared with that in the adjacent normal breast tissues (P

MicroRNAs (miRNAs) are small, non-coding RNAs that modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. The aim of this study was to investigate the expression of microRNA-145 (miR-145) in human papillary thyroid cancer and its potential function. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to determine the expression level of miR-145 in ten papillary thyroid cancer and adjacent normal specimens. The function of miR-145 overexpression on the proliferation of human TPC1 thyroid cancer cells was conducted by MTT assays and by colony-formation assays. Western blot was used to validate the impact of miR-145 on the protein expression of the target gene. Luciferase reporter assays were employed to validate a putative target of miR-145. MiR-145 expression was relatively decreased in papillary thyroid cancer specimens compared with adjacent normal tissues (P

Many studies have demonstrated that microRNAs (miRNAs) may play vital roles in the development of breast cancer. The aim of this study was to examine the expression levels of miR-497 in human breast cancer and investigate whether its potential roles involved targeting Bcl-2. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to examine the expression levels of miR-497 in 48 breast cancer specimens and six breast cancer cell lines. MTT assay, colony formation assay, and flow cytometry were conducted to explore the potential functions of miR-497 in human MDA-MB-231 breast cancer cells. Correlation analysis and dual-luciferase reporter assay were performed to validate whether Bcl-2 was a direct target of miR-497. The effects of modulating miR-497 on endogenous levels of Bcl-2 were subsequently confirmed via qRT-PCR and western blot. MTT assay, colony formation assay and flow cytometry were used to indicate the roles of endogenous Bcl-2 in breast cancer cells. miR-497 expression levels were significantly decreased in human breast cancer specimens and cell lines (P

Background. Fine needle aspiration cytology (FNAC) and fine needle nonaspiration cytology (FNNAC) are useful cost-effective techniques for preoperatively assessing thyroid lesions. Both techniques have advantages and disadvantages, and there is controversy over which method is superior. This meta-analysis was performed to evaluate the differences between FNAC and FNNAC for diagnosis of thyroid nodules.Methods. Primary publications were independently collected by two reviewers from PubMed, Web of Science, Google Scholar, EBSCO, OALib, and the Cochrane Library databases. The following search terms were used: fine needle, aspiration, capillary, nonaspiration, sampling without aspiration, thyroid, and cytology. The last search was performed on February 1, 2015.Results. Sixteen studies comprising 1,842 patients and 2,221 samples were included in this study. No statistically significant difference was observed between FNAC and FNNAC groups with respect to diagnostically inadequate smears, diagnostically superior smears, diagnostic performance (accuracy, sensitivity, specificity, negative predictive value, and positive predictive value), area under the summary receiver operating characteristic curve, average score of each parameter (background blood or clot, amount of cellular material, degree of cellular degeneration, degree of cellular trauma, and retention of appropriate architecture), and total score of five parameters.Conclusion. FNAC and FNNAC are equally useful in assessing thyroid nodules.

Background and aim: Protein Kinase (casein kinase 2, CK2) is a pleiotropic serine-threonine kinase that is frequently dysregulated in many human tumors; microRNAs (miRNAs) are a class of small noncoding RNAs which play important roles in human cancers. This study aimed to investigate the role of CK2 and miRNA expression in breast cancer. Methods: Casein kinase 2 in MCF-7 breast cancer cell line was inhibited by the CK2 inhibitor TBB (4,5,6,7-tetrabromobenzotriazole), then cell proliferation was studied using MTT assay, and cell cycle distribution and apoptosis were detected by flow cytometry. The alteration of microRNAs expression profile was determined by microarray technology, followed by RT-PCR confirmation. Results: Here, we for the first time showed that inhibition of CK2 in MCF-7 breast cancer cells causes suppressed cell growth, which was related with dysregulation of the miRNA profile and altered expression. CK2 inhibition induced the up-regulated expression of 17 miRNAs and 10 down-regulated microRNAs which contributed to the impaired growth, inhibited cell cycle progress and increased apoptosis of MCF-7 cells by a CK2 inhibitor. Conclusions: These findings highlight the potential role of dysregulated miRNA expression regulated by CK2 in breast cancer.