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Objectives: This study concentrates on exploring the synergistic effect of shikonin on cisplatin against oral cancer. Methods: To analyze the IC50 value of shikonin, gradient concentrations of shikonin were added to the oral cancer cell culture medium. After the cisplatin‐resistant cell line was established, the effects of cisplatin and shikonin on the survival rate, proliferation, apoptosis and related pathway protein expression of common/drug‐resistant oral cancer cells were compared through MTT, clone formation, flow cytometry, and Western blot experiments. β‐catenin, which had the most significant expression changes, was overexpressed and silenced, and used to design a reverse validation. Results: Shikonin inhibited the viability of oral cancer cells. Although cisplatin killed some cancer cells, its effect on drug‐resistant cancer cells was significantly reduced. The addition of shikonin enhanced the sensitivity of drug‐resistant cells to cisplatin. Shikonin regulated key proteins in cell proliferation and apoptosis‐related pathways. Among them, shikonin generated the most evident inhibitory effect on β‐catenin. Therefore, β‐catenin overexpression plasmid/siβ‐catenin was transfected into the cells. Silenced β‐catenin was found to reinforce the damaging effect of cisplatin on cancer cells, and overexpressed β‐catenin reversed the effect of shikonin. Conclusion: By down‐regulating β‐catenin expression, shikonin improves the sensitivity of drug‐resistant oral cancer cells to cisplatin. [ABSTRACT FROM AUTHOR]

Long nanopore reads are advantageous in de novo genome assembly. However, nanopore reads usually have broad error distribution and high-error-rate subsequences. Existing error correction tools cannot correct nanopore reads efficiently and effectively. Most methods trim high-error-rate subsequences during error correction, which reduces both the length of the reads and contiguity of the final assembly. Here, we develop an error correction, and de novo assembly tool designed to overcome complex errors in nanopore reads. We propose an adaptive read selection and two-step progressive method to quickly correct nanopore reads to high accuracy. We introduce a two-stage assembler to utilize the full length of nanopore reads. Our tool achieves superior performance in both error correction and de novo assembling nanopore reads. It requires only 8122 hours to assemble a 35X coverage human genome and achieves a 2.47-fold improvement in NG50. Furthermore, our assembly of the human WERI cell line shows an NG50 of 22 Mbp. The high-quality assembly of nanopore reads can significantly reduce false positives in structure variation detection. Nanopore reads have been advantageous for de novo genome assembly; however these reads have high error rates. Here, the authors develop an error correction and de novo assembly tool, NECAT, which produces efficient, high quality assemblies of nanopore reads. [ABSTRACT FROM AUTHOR]

Background: Soy food intake may have protective effects against the risk for breast cancer, including estrogen receptor (ER)-negative breast cancer. However, the underlying molecular mechanisms remain unclear.Methods: To evaluate the association of soy intake with the expression of microRNAs (miRNAs) and genes in the tumor tissue of patients with triple-negative breast cancer (TNBC; ie, breast cancer lacking expression of ER, progesterone receptor, and human epidermal growth factor receptor 2), the expression of 800 miRNAs and 302 genes were measured with NanoString nCounter assays in formalin-fixed, paraffin-embedded tumor tissue from 272 TNBC patients. Soy intake during the 1-year period before the cancer diagnosis was assessed with a validated food-frequency questionnaire. The association of soy intake with the expression of miRNAs and genes was evaluated via linear regression analysis with adjustments for patient age and TNM stage.Results: A total of 14 miRNAs and 24 genes were significantly associated with soy food intake (P < .05): Thirteen of the 14 miRNAs (92.9%) and 9 of the 24 genes (37.5%), including tumor suppressors miR-29a-3p and IGF1R, showed overexpression for those women with high soy intake, whereas the remaining miRNAs and genes, including oncogenes KRAS and FGFR4, showed underexpression. Furthermore, cell growth-related genes showed a predominantly underexpression pattern according to a comparison of tumor samples from women with high soy food intake and samples from women with lower soy food intake.Conclusions: This study suggests that long-term prediagnosis soy intake may lead to increased expression of tumor suppressors and decreased expression of oncogenes, especially cell growth-related genes, in breast tumor tissues. Cancer 2016;122:2544-51. © 2016 American Cancer Society. [ABSTRACT FROM AUTHOR]