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Citrus plants are natural hosts of five viroid species and large numbers of sequence variants. In this paper a simple and sensitive one step multiplex RT-PCR protocol with an internal control was utilised to simultaneously detect and differentiate five citrus viroids: Citrus exocortis viroid (CEVd), Citrus bent leaf viroid (CBLVd), Hop stunt viroid (HSVd), Citrus viroid-III (CVd-III) and Citrus viroid-IV (CVd-IV). In addition, a micro and rapid total nucleic acid extraction method was developed and the protocol applied to evaluate the occurrence and distribution of citrus viroids in China.

Objective. This study explored the colorectal cancer exosome lncRNA prostate cancer associated transcript 1– (PCAT1) mediated circulating tumors and the mechanism of cell colorectal cancer liver metastasis. Methods. Exosomes were extracted from the primary colorectal cancer (CRC) cell lines HCT116 and SW480 and cultured with T84 and human umbilical vein endothelial (HUVE) cells. The expression of PCAT1 and miR-329-3p was detected by real-time quantitative polymerase chain reaction (RT-qPCR), the expression of Netrin-1, CD146, and epithelial mesenchymal transition (EMT) related proteins was detected by Western blot, the proliferation activity of T84 cells was detected by cell counting kit 8 (CCK-8), and cell migration was detected by Transwell. The expression of the F-actin signal was detected by immunofluorescence after coculture of exosomes with human umbilical vein endothelial cells (HUVECs). Changes in subcutaneous tumor and liver nodule size after PCAT1 deletion were observed in a mouse model of liver metastasis from rectal cancer. Results. PCAT1 expression was upregulated in primary cell lines and their exosomes. After exosomes were cocultured with colorectal cancer tumor circulating T84 cells, the expression of Netrin-1 and CD146 was upregulated, the expression of miR-329-3p was downregulated, the proliferation and migration ability of T84 cells were enhanced, and EMT occurred. After knocking down PCAT1, the above phenomenon was reversed. Similarly, after exosomes were cocultured with HUVECs, the expression of the F-actin signal increased, and after PCAT1 was knocked down, the F-actin signal also decreased. PCAT1 regulates miR-329-3p/Netrin-1 and affects the biological behavior of T84 and F-actin signal expression in HUVECs. In a mouse model of colorectal cancer liver metastasis, knocking down PCAT1 significantly reduced the nodules formed by liver metastasis in mice. Conclusions. LncRNA PCAT1 derived from colorectal cancer exosomes regulates the activity of the Netrin-1-CD146 complex in circulating tumor cells (CTCs) to promote the occurrence of colorectal cancer EMT and liver metastasis and provides new molecular targets for the treatment of colorectal cancer liver metastasis.

CCCTC-binding factor (CTCF), a ubiquitously expressed and highly conserved protein, is known to play a critical role in chromatin structure. Post-translational modifications (PTMs) diversify the functions of protein to regulate numerous cellular processes. However, the effects of PTMs on the genome-wide binding of CTCF and the organization of three-dimensional (3D) chromatin structure have not been fully understood. In this study, we uncovered the PTM profiling of CTCF and demonstrated that CTCF can be O-GlcNAcylated and arginine methylated. Functionally, we demonstrated that O-GlcNAcylation inhibits CTCF binding to chromatin. Meanwhile, deficiency of CTCF O-GlcNAcylation results in the disruption of loop domains and the alteration of chromatin loops associated with cellular development. Furthermore, the deficiency of CTCF O-GlcNAcylation increases the expression of developmental genes and negatively regulates maintenance and establishment of stem cell pluripotency. In conclusion, these results provide key insights into the role of PTMs for the 3D chromatin structure. CTCF, which is known to play critical role in chromatin structure, undergoes post-translational modifications (PTMs). In this research, O-GlcNAcylation was found to inhibit CTCF binding, impacting 3D chromatin structure, gene expression and cellular development.

Mobile edge computing (MEC) utilizes wireless access network to provide powerful computing resources for mobile users to improve the user experience, which mainly includes two aspects: time and energy consumption. Time refers to the latency consumed to process user tasks, while energy consumption refers to the total energy consumed in processing tasks. In this paper, the time and energy consumption in user experience are weighted as a mixed overhead and then optimized jointly. We formulate a mixed overhead of time and energy (MOTE) minimization problem, which is a nonlinear programming problem. In order to solve this problem, the block coordinate descent method to deal with each variable step by step is adopted. We further analyze the minimum value of delay parameters in the model, and examine two special cases: 1-offloading and 0-offloading. In 1-offloading, all the task data is offloaded to MEC server, and no data offloaded in 0-offloading. The necessary and sufficient conditions for the existence of two special cases are also deduced. Besides, the multi-user situation is also discussed. In the performance evaluation, we compare MOTE with other offloading schemes, such as exhaustive strategy and Monte Carlo simulation method-based strategy to evaluate the optimality. The simulation results show that MOTE always achieves the minimal overhead compared to other algorithms.

Long non-coding RNS (lncRNA) GATA6-AS regulates endothelial cell growth, which is involved in many types of human diseases. Our study was carried out to investigate the involvement of GATA6-AS in gallbladder cancer (GBC). Sixty-two patients with GBC were recruited in this study. PCR analysis was performed to determine the expression of GATA6-AS, miR-421 and TIMP-2 in tissues or cell lines. Transwell migration and invasion assay was applied. We found that GATA6-AS was downregulated in tumor tissues than in adjacent healthy tissues of GBC patients, and GATA6-AS expression levels in tumor tissues decreased with the increase of clinical stages. MiR-421 was upregulated in tumor tissues than in adjacent healthy tissues of GBC patients and was inversely correlated with the expression levels of GATA6-AS. MiR-421 overexpression failed to significantly affect GATA6-AS in GBC cells, while GATA6-AS overexpression resulted in inhibited miR-421 expression. GATA6-AS overexpression led to decreased migration and invasion rates of GBC cells. MiR-421 overexpression led to increased migration and invasion rates of GBC. Rescue experiments (co-transfection) showed that miR-421 overexpression led to attenuated effects of GATA6-AS overexpression. GATA6-AS may inhibit cancer cell migration and invasion in GBC by downregulating miR-421.

Cell division cycle 25A (CDC25A) is a core regulator of the cell cycle that has a dual-specific phosphatase activity, which is closely associated with the occurrence and development of a tumor, and is overexpressed in liver cancer. However, the molecular mechanism of CDC25A in the development of liver cancer remains unclear. The purpose of the present study was to further investigate the effect of CDC25A on cell proliferation in vitro and in vivo and to investigate whether an interaction exists between CDC25A and interleukin (IL)-6 in liver cancer. An Affymetrix human gene expression profiling chip screened differentially expressed genes in HepG2 cells with silenced CDC25A and the IL-6 signaling pathway was revealed to be significantly inhibited (P<0.05). In the present study, the effects of CDC25A on cell proliferation and migration were analyzed using cell cycle, MTT and Transwell assays. Reverse transcription-quantitative PCR, western blot and immunohistochemistry analyses confirmed that silencing the CDC25A gene downregulated the expression of IL-6 in HepG2 cells and the mRNA and protein expression of IL-1β, mitogen-activated protein kinase kinase kinase 14 (NIK) and nuclear factor-κB (NF-κB), which are regulatory molecules upstream of IL-6. In addition, silencing CDC25A by short hairpin RNA inhibited the development of liver cancer xenograft tumor types in nude mice, and decreased the expression of IL-1β, NIK, NF-κB and IL-6 in xenograft tumor types. In conclusion, silencing CDC25A significantly inhibited the proliferation of liver cancer cells in vitro and in vivo, potentially via an interaction with IL-6 through the downregulation of the IL-1β/NIK/NF-κB signaling axis.

The optimal induction chemotherapy regimens for young adult patients with newly diagnosed acute myeloid leukemia (AML) are not well-defined since the lack of direct comparisons between emerging treatments. Network meta-analysis (NMA) is a statistical tool to integrate direct and indirect evidence to evaluate the effect of multiple interventions. Thus, we conducted an NMA to systematically assess the efficacy and safety of different inductions for these patients. PubMed, Embase, Cochrane Library, and Web of Science were searched from establishment to 2020–03-11. Randomized controlled trials (RCTs) using different inductions were included. We deemed 11 trials eligible, including 11 inductions with 5052 participants. Relative risk (RR) and 95% confidence intervals (CIs) were calculated. In terms of complete remission (CR) rate, DAC ranked highest and was significantly higher than IA (RR = 1.27, 95% CI (1.09–1.48)) and DA (RR = 1.28, 95% CI (1.13–1.46)) (p < 0.05). The ranking of DA + Pioglitazone was second only to that of DAC, followed by HAA. For early mortality, HAD, HAA, and DA + GO were significantly higher than DA/IA (p < 0.05). DAC and DA + Pioglitazone showed similar early mortality compared to DA/IA (p > 0.05). Regarding incidence of early grade 3–4 infection, no significant differences between interventions were observed. To conclude, among the included 11 induction regimens, DAC was potentially the top choice for young adult patients with newly diagnosed AML, with highest CR rate, low early mortality, and incidence of early infection. DA + Pioglitazone and HAA also showed a superiority over the others to achieve higher CR rate, while caution should be kept in mind due to the higher early mortality of HAA.

This network meta-analysis was conducted to compare the predictive value of eight SNPs on the efficacy of antidepressants in major depressive disorder (MDD), including 5-HTTLPR,  (rs6311, rs6314, rs7997012 and rs6313),  (rs6295),  (rs6265) and 5HTTSTin2. Databases were searched for related studies published up to December 2019. A total of 16 studies were included in this study. The predictive value were evaluated by the use of the odd ratios (OR) and drawing surface under the cumulative ranking curves (SUCRA). The pairwise meta-analysis indicated that in terms of overall response ratio, the SNPs were not associated with the efficacy of antidepressants in MDD. The result of this network meta-analysis suggested that there was no significant difference in predictive value of eight SNPs on the efficacy of antidepressants in MDD. More research is needed to explore the relationship between SNPs and antidepressant response.

Epigallocatechin gallate (EGCG), the most active monomer in green tea (GT), has demonstrated potential therapeutic and preventive effects on various tumors, including liver cancer. However, the anticancer mechanisms of EGCG in liver cancer remain to be elucidated. The abnormal expression of cell division cycle 25A (CDC25A) has been identified in liver cancer and is closely associated with malignancy and poor prognosis in patients with hepatocellular carcinoma (HCC). The present study used human hepatoma cell lines and rats with diethylnitrosamine (DEN)-induced HCC as models to investigate the association between the effect of EGCG on liver cancer and regulation of the p21waf1/Cip1/CDC25A axis. The results demonstrated that EGCG can inhibit the proliferation of HepG2 and Huh7 cells, reduce the expression of CDC25A and increase the expression of p21waf1/Cip1 in HepG2. In vivo, HCC was induced by DEN in Sprague-Dawley rats. EGCG significantly reduced tumor volume and improved the survival rates of rats with HCC. The expression levels of CDC25A mRNA and protein in liver tissues and the level of serum γ glutamyl transpeptidase in rats treated with EGCG were significantly decreased, while p21waf1/Cip1 mRNA and protein expression levels were increased compared with the HCC group, in the process of DEN-induced HCC. No significant difference in the chemopreventive effects on liver cancer was observed between GT extract and EGCG under an EGCG equivalence condition. Thus, EGCG can suppress human hepatoma cell proliferation and prolong the survival of rats with HCC, and the potential mechanism may be involved in EGCG-induced upregulation of p21waf1/Cip1 and downregulation of CDC25A.