Current extraction methods often extract DNA and RNA separately, and few methods are capable of co-extracting DNA and RNA from sputum. We established a nucleic acid co-extraction method from sputum based on magnetic beads and optimized the method by evaluating influencing factors, such as the guanidinium thiocyanate (GTC) and dithiothreitol (DTT) concentrations, magnetic bead amount, incubation temperature, lysis buffer pH and RNA carrier type. The feasibility of the simultaneous nucleic acid co-extraction method was evaluated by amplifying DNA and RNA viruses from a single clinical specimen with a multiplex RT-qPCR method. Both DNA and RNA were most efficiently extracted when the GTC and DTT concentrations were 2.0 M and 80 mM, respectively, 20 μl magnetic beads were added, the incubation temperature was 80 °C, the pH was 8 or 9, and RNA carrier A was used. Therefore, we established a simple method to extract nucleic acids from two important respiratory viruses compared with other commercial kits. This magnetic beads-based co-extraction method for sputum followed by a multiplex RT-qPCR can rapidly and precisely detect DNA and RNA viruses from a single clinical specimen and has many advantages, such as decreased time, low cost, and a lack of harmful chemicals.

MicroRNAs (miRNAs) have recently been shown to down-regulate gene expression by targeting mRNA translation and to play a critical role in tumorigenesis; how they regulate bladder tumor development, particularly in patients, is, however, poorly understood. The difference in miRNA expression in a bladder tumor compared with healthy tissue from the same patients was examined using microRNA arrays in seven patients. Here, we showed that up-regulation of miRNA was not commonly found in this limited number of patients, and four miRNAs (miR-26a, miR-29c, miR-30c, miR-30e-5p) were down-regulated as a common marker in patients with a 1-3 grade of disease. Our data suggest that instead of up-regulation of carcinogenic miRNAs, loss of regulation of these miRNA may be critical for bladder tumor development in patients.

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Cervical cancer is the fourth most common cancer in women globally. Lack of effective pharmacotherapies for cervical cancer mainly attributed to an elusive understanding of the mechanism underlying its pathogenesis. Pyroptosis plays a key role in inflammation and cancer. Our study identified microRNA (miR) 145 (miR-145)/gasdermin D (GSDMD) signaling pathway as critical mediators in the effect of tanshinone II A on HeLa cells. In the present study, we found that treatment of tanshinone II A led to an obvious repression of cell proliferation and an increase in apoptosis on HeLa cells, especially in high concentration. Compared with the controlled group, tanshinone II A enhanced the activity of caspase3 and caspase9. Notably, the results demonstrated that tanshinone II A regulated cell proliferation of HeLa cells by regulating miR-145/GSDMD signaling pathway. Treatment of tanshinone II A significantly up-regulated the expression of GSDMD and miR-145. After transfection of si-miR-145 plasmids, the effects of tanshinone II A on HeLa cells were converted, including cell proliferation, apoptosis and pyroptosis. In addition, the results showed that tanshinone II A treatment altered the expression level of PI3K, p-Akt, NF-kB p65 and Lc3-I. Collectively, our findings demonstrate that tanshinone II A exerts anticancer activity on HeLa cells by regulating miR-145/GSDMD signaling. The present study is the first time to identify miR-145 as a candidate target in cervical cancer and show an association between miR-145 and pyroptosis, which provides a novel therapy for the treatment of cervical cancer.

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Background: Studies have shown inconsistent results regarding the diagnostic performance of ultrasound elastography for axillary lymph node metastasis (ALNM) in breast cancer. This meta-analysis aimed to estimate the diagnostic performance of ultrasound elastography (divided into quantitative and qualitative elastography) for ALNM in patients with breast cancer. Methods: The PubMed and Embase databases were searched for eligible studies exploring the diagnostic performance of ultrasound elastography for ALNM in patients with breast cancer. The included studies were divided into quantitative and qualitative elastography groups to perform separate meta-analyses. The diagnostic performance was investigated with pooled sensitivity and specificity and diagnostic odds ratio (DOR) using a bivariate mixed-effects regression model. A summary receiver operating characteristic curve was constructed, and the area under the curve (AUC) was calculated. Results: Seven and 11 studies were included in the quantitative and qualitative elastography meta-analyses, respectively. The pooled sensitivity and specificity, DOR, and AUC with their corresponding 95% confidence intervals were 0.82 (0.75, 0.87), 0.88 (0.78, 0.93), 33 (13, 83), and 0.89 (0.86, 0.91), respectively, for quantitative elastography and 0.81 (0.69, 0.89), 0.92 (0.79, 0.97), 46 (12, 181), and 0.92 (0.89, 0.94), respectively, for qualitative elastography. No significant publication bias existed. Fagan plots demonstrated good clinical utility. However, substantial heterogeneity existed among studies. Study design, measurement, and reference standard served as potential sources of heterogeneity for quantitative studies, which were measurement and reference standard for qualitative studies. Conclusions: Both quantitative and qualitative elastography seem to be feasible, non-invasive diagnostic tools for ALNM in breast cancer. Nevertheless, the results Huang et al. Meta-Analysis of Elastography for ALNM must be interpreted carefully, paying attention to heterogeneity issues, especially for quantitative elastography studies.

Propofol, a commonly used intravenous anesthetic agent during surgery, has relatively widespread pharmacological actions. Previous studies have reported that propofol may act as an antitumor drug in several cancer types, such as pancreatic cancer, lung cancer and gastric cancer. However, the underlying mechanism in ovarian cancer remain unknown. Therefore, the present study investigated the pharmacological effect of propofol on micrornas (mirnas) in ovarian cancer treatment. Propofol (1, 5 or 10 µg/ml) was used to treat a2780 and SKoV3 ovarian cancer cells for 1, 2, 3, 4 or 5 days. The MTT assay was used to detect cell viability, while wound healing and Transwell assays were utilized to assess the invasive and migratory abilities. The bioinformatics prediction approach identified differentially expressed miRNAs (miRs) that were used in Gene ontology, Gene Set enrichment analysis and Kyoto encyclopedia of Genes and Genomes analyses. The expression levels of miR-125a-5p and lin-28 homolog B (lin28B) were evaluated by reverse transcription-quantitative Pcr (rT-qPcr). a luciferase assay was performed to identify the relationship between mir-125a-5p and lin28B. Western blotting was conducted to measure the protein expression of LIN28B. It was demonstrated that propofol significantly upregulated miR-125a-5p to exert its antitumor activity. rT-qPcr results suggested that propofol could upregulate miR-125a-5p and LIN28B expression levels in ovarian cancer cell lines. Western blot analysis also indicated that propofol could enhance the expression of LIN28B in ovarian cancer cell lines. The luciferase assay identified that miR-125a-5p could directly inhibit the expression of LIN28B to suppress proliferation and metastasis in ovarian cancer. in conclusion, these results suggested that propofol inhibited ovarian cancer proliferation and metastasis by enhancing mir-125a-5p, which targets lin28B.

Ovarian cancer is a major gynecologic cancer and common cause of gynecologic cancer death worldwide. However, the molecular mechanisms of ovarian cancer progression are still unclear. circular RNAs (circRNAs) are recently reported to be involved in cancer progression regulation but the potential functions of circRNAs in ovarian cancer remains unknown. In this study, we explored the expression of circKIF4A in ovarian cancer tissues. Then, a series of experiments were conducted to investigate how circKIF4A functioned in ovarian cancer in vitro and in vivo . The results revealed that circKIF4A was highly expressed in ovarian cancer tissues. Knockdown of circKIF4A suppressed cell proliferation and migration in ovarian cancer. Subsequent mechanism study revealed that circKIF4A acted as a competitive endogenous RNA (ceRNA) to promoted ovarian cancer progression by sponging miR-127 and upregulated the expression of Junctional adhesion molecule 3 (JAM3). Therefore, circKIF4A could be a novel biomarker and therapeutic target for ovarian cancer.