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The purpose of our study is to clarify the effects of microRNA-129-5p (miR-129-5p) in cellular processes correlated with cancer development and progression of Glioblastoma (GBM) cell by regulating FNDC3B. MiR-129-5p and FNDC3B expression in GBM tissues and tumor adjacent tissues were tested by quantitative real-time PCR. We validated the target relationship between miR-129-5p and FNDC3B by dual luciferase reporter gene system. MTT, colony formation, flow cytometry, Transwell and wound healing assays were used to analyze cell viability, proliferation, apoptosis, invasiveness and migration. The level of FNDC3B protein expression was detected by Western Blot. MiR-129-5p was downregulated in GBM tissues and cell lines, while FNDC3B was upregulated in GBM tissues. The result of luciferase reporter gene assay demonstrated that miR-129-5p could target FNDC3B by binding to the 3′ UTR. The overexpression of miR-129-5p or the inhibition of FNDC3B can both inhibit U87 cell viability, proliferation, migration and invasion, while promote cell apoptosis. Our results suggested that miR-129-5p could directly suppress FNDC3B, which might be one of potential mechanisms in inhibiting cell processes including viability, proliferation, migration and invasiveness of U87 cells. [ABSTRACT FROM AUTHOR]

Abstract: A nonlinear Schrödinger equation with external field is obtained for nonlinear optics in a non-homogeneous medium. On the basis of the Melnikov function and KAM theory, the complexity of the wave propagation of the equation is studied in the case of weak periodic external field. [Copyright &y& Elsevier]

A method for obtaining first integrals and integrating factors of n-th order autonomous systems is proposed. The search for first integrals and integrating factors can be reduced to the search for a class of invariant manifolds of the systems. Finally, the proposed method is applied to Euler-Poisson equations (gyroscope system), and the fourth first integral of the system in general Kovalevskaya case can be obtained. [Copyright &y& Elsevier]

The dynamics of multiple ecosystem functions (that is, multifunctionality) are closely associated with biodiversity, often show positive relationships, but the dynamics of the biodiversity multifunctionality relationship along soil profiles remain unclear. Eutrophication significantly affects biodiversity and soil functions, whereas the mechanisms underlying the impact of nitrogen addition on the biodiversity multifunctionality relationship are poorly understood. Here, we conducted a common garden experiment manipulating plant diversity and nitrogen addition to quantify the effects of biodiversity on soil multifunctionality in the topsoil and subsoil under different nitrogen addition levels. We showed that nitrogen addition had a minor impact on soil multifunctionality but weakened the positive biodiversity multifunctionality relationship. We also found that the positive plant diversity effect on soil multifunctionality decreased with soil depths, resulting in a weaker biodiversity multifunctionality relationship in the subsoil. The weak biodiversity multifunctionality relationship in the subsoil was caused by weakening the relationship between aboveground biomass and soil multifunctionality; nitrogen addition weakened the biodiversity multifunctionality relationship through the attenuation of the association of aboveground biomass and soil microbes with multifunctionality. Our study demonstrates that nitrogen addition undermines the biodiversity soil multifunctionality relationship and the relationship is weakened along the soil profiles, suggesting that Earth system models must represent these heterogeneous soil dynamics to accurately predict future feedbacks to global changes. • N addition weakens biodiversity soil multifunctionality (SMF) relationships (BMR). • Decrease in aboveground biomass (AGB) inputs leads to a weak BMR in the subsoil. • Weak associations of AGB and soil microbes with SMF weaken the BMR under N addition. [ABSTRACT FROM AUTHOR]

Ion channel is an integral membrane protein that allows the permeation of charge ions across hydrophobic phospholipid membranes, including plasma membranes and organelle membranes (such as mitochondria, endoplasmic reticulum and vacuoles), which are widely distributed in various cells and tissues, such as cardiomyocytes, smooth muscle cells, and nerve cells. Ion channels establish membrane potential by regulating ion concentration and membrane potential. Membrane potential plays an important role in cells. Studies have shown that ion channels play a role in a number of immune-related diseases caused by functional defects in ion channels on immune or non-immune cells in major human organs, usually affecting specific organs or multiple organs. The present review discusses the relationship between ion channels and immune diseases in major organs of the human body. [ABSTRACT FROM AUTHOR]

The upper gastrointestinal (GI) tumors are multifactorial diseases associated with a combination of oncogenes and environmental factors. Currently, surgery, chemotherapy, radiotherapy and immunotherapy are relatively effective treatment options for the patients with these tumors. However, the asymptomatic phenotype of these tumors during the early stages poses as a significant limiting factor to diagnosis and often renders treatments ineffective. Therefore, new early diagnosis and effective therapy for upper GI tumors are urgently needed. Ca2+ is a pivotal intracellular second messenger and plays a crucial role in living cells by regulating several processes from cell division to death. The aberrant Ca2+ homeostasis is related to many human pathological conditions and diseases, including cancer, and thus the changes in the expression and function of plasma membrane Ca2+ permeable channels and sodium/calcium exchangers are frequently described in tumorigenesis and tumor development of the upper GI tract, including voltage-gated Ca2+ channels (VGCC), transient receptor potential (TRP) channels, store-operated channels (SOC) and Na+/Ca2+ exchanger (NCX). This review will summarize the current knowledge about plasma membrane Ca2+ permeable channels and sodium/calcium exchangers in the upper GI tumors and provide a synopsis of recent advancements on the role and involvement of these channels in upper GI tumors as well as a discussion of the possible strategies to target these channels and exchangers for diagnosis and therapy of the upper GI tumors. • Voltage-gated Ca2+ channels (VGCC), transient receptor potential (TRP) channels, store-operated channels (SOC) and Na+/Ca2+ exchanger (NCX) involve in the tumorigenesis and development of the upper gastrointestinal tract. • Ca2+ permeable channels and sodium/calcium exchangers present abnormal expression and activity in upper gastrointestinal tumors. • Calcium channels can be used as a promising diagnostic biomarkers and therapeutic targets for esophageal cancer and gastric cancer. [ABSTRACT FROM AUTHOR]

Abstract Glucocorticoid hormones have been widely used in clinical practice as potent anti-inflammatory and immunosuppressive agents. However, the underlying mechanisms of how they work remain unaddressed. Here, we used RNA-set to profile spleen gene expression in adult mice after consistent intraperitoneal injection of dexamethasone. We identified 13565 genes in control (injected with 0.9% NaCl) and 13702 genes in dexamethasone-injected group, 12920 genes were expressed in both, but 645 genes were identified only in control and 782 genes were identified only in the dexamethasone group. In the dexamethasone-injected group 101 and 67 genes were down-and up-regulated, respectively. Among these, 129 were coding genes, 19 were identified as non-coding genes or pseudogenes, and the remaining 20 were TEC (to be experimentally confirmed) genes. Gene ontology (GO) and KEGG pathway analysis revealed that the cytokine-cytokine receptor interaction pathway was highly enriched in these differentially expressed genes, and that a majority of the 129 identified coding genes were involved in immune system and cell adhesion-associated processes. Moreover, systemic lupus erythematosus, renin-angiotensin system, fat digestion and absorption, and glycerolipid metabolism pathways were significantly affected in the dexamethasone-treatment group. No obvious signaling pathway was enriched in the control group. Additionally, 20 immunoglobulin heavy or light chain variable region genes (IGH(L)Vs) were down regulated in the dexamethasone-injected group. IGH(L)Vs encode the variable region of immunoglobulin heavy chain and determine the diversity and specificity of antibodies. We were unable to determine the function of the 19 non-coding genes with differential expression following dexamethasone treatment. Our findings indicate that the expression of IGH(L)Vs and non-coding genes play an important role in the anti-inflammatory and immunosuppressive effects of dexamethasone and could be developed as potential agents in clinical practice. Highlights • Long-term, high dose dexamethasone treatment changes gene expression in the spleen. • RNA-Seq showed 20 down-regulated IGH(L)V family genes in the treatment group. • IGH(L)Vs and non-coding genes are involved in dexamethasone-induced effects. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma is the most common type of liver cancer and associated with a high fatality rate. This disease poses a major threat to human health worldwide. A considerable number of genetic and epigenetic factors are involved in the development of hepatocellular carcinoma. However, the molecular mechanism underlying the progression of hepatocellular carcinoma remains unclear. Karyopherin subunit alpha 2 (KPNA2), also termed importin α1, is a member of the nuclear transporter family. In recent years, KPNA2 has been gradually linked to the nuclear transport pathway for a variety of tumor-associated proteins. Furthermore, it promotes tumor development by participating in various pathophysiological processes such as cell proliferation, apoptosis, immune response, and viral infection. In hepatocellular carcinoma, it has been found that KPNA2 expression is significantly higher in liver cancer tissues versus paracancerous tissues. Moreover, it has been identified as a marker of poor prognosis and early recurrence in patients with hepatocellular carcinoma. Nevertheless, the role of KPNA2 in the development of hepatocellular carcinoma remains to be determined. This review summarizes the current knowledge on the pathogenesis and role of KPNA2 in hepatocellular carcinoma, and provides new directions and strategies for the diagnosis, treatment, and prediction of prognosis of this disease. [ABSTRACT FROM AUTHOR]

• SELS promotes tumor progression and inhibits apoptosis in ccRCC cells. • SELS inhibits the migration of ccRCC cells through modulating EMT process. • SELS stabilizes c-Myc by preventing ubiquitin–proteasome-mediated degradation. Clear cell renal cell carcinoma (ccRCC) is one of the most lethal genitourinary tumors with rapid progression and metastasis. Selenoprotein S (SELS), which is broadly expressed in human tissues, has been reported to be involved in ER homeostasis and inflammation. However, the biological roles of SELS in ccRCC remain unclear. In this study, we found that SELS expression was significantly higher in ccRCC and correlated with multiple clinicopathological features. Overexpression of SELS could promote cell proliferation and inhibit apoptosis in 786-O cells, whereas silence of SELS elicited opposite effect. Further mechanistic studies revealed that SELS enhanced cell proliferation and inhibited apoptosis through activating AKT/GSK3β/NF-κB signaling pathway. Besides, SELS could stabilize c-Myc by preventing ubiquitin–proteasome-mediated degradation. Interestingly, we found that SELS could also inhibit migration of ccRCC cell likely through repressing epithelial–mesenchymal transition (EMT). Collectively, our findings suggested that SELS promoted tumor progression, and inhibited apoptosis and migration through AKT/GSK3β/NF-κB signaling pathway and EMT in ccRCC. [ABSTRACT FROM AUTHOR]

• A1CF increases DKK1 expression and activates ERK pathway. • A1CF promotes proliferation and colony formation of 786-O cells. • A1CF activates ERK signaling pathway via DKK1. • A1CF-DKK1 signal axis promotes RCC cell proliferation through ERK signaling. The function and mechanism of RNA editing proteins have been extensively studied, but its association with cellular processes and signaling pathways remained unaddressed. Here, we explored the function of RNA editing complementary protein- Apobec-1 Complementation Factor (A1CF) in the proliferation and colony formation of renal cell carcinoma (RCC) cells. Decreased A1CF expression inhibits the proliferation and colony formation of 786-O cells; and further signaling pathway screening demonstrated that A1CF increases ERK activation and DKK1 expression. Moreover, knockdown of DKK1 has similar phenotypes with A1CF deficiency in 786-O cells on cell proliferation and colony formation and ERK activation. Decreasing of DKK1 expression reduces the phosphorylation of ERK1/2 and MEK1/2 increased by A1CF overexpression; further, inhibiting of the phosphorylation of MEK1/2 by U0126 also decreases the ERK activation upregulated by A1CF overexpression. Deficiency of DKK1 or U0126 treatment suppresses the cell proliferation promoted by A1CF overexpression in 786-O cells; furthermore, U0126 treatment inhibits DKK1-increased cell proliferation in 786-O cells. Our results reveal that DKK1 mediates A1CF to activate ERK in promotion renal carcinoma cell proliferation and colony formation. For the important function of ERK signaling pathway in tumor metastasis and key position of DKK1 in Wnt signaling pathway, we associate RNA editing protein-A1CF with multiple cellular processes and signaling pathways through DKK1, and the key node of A1CF-DKK1-MEK/ERK axis is a potential targeting site for RCC therapy. [ABSTRACT FROM AUTHOR]

Cytosolic calcium [Ca2+] cyt signaling plays a critical role in the regulation of multiple cellular functions, and Ca2+ channels/transporters are important to regulate calcium homeostasis whose abnormality may contribute human tumorogenesis including colorectal cancer (CRC). In this review, we summarized and discussed the current knowledge on pathogenic roles of the altered [Ca2+] cyt and Ca2+ channels/transporters like SOCE, TRP channels, SERCA and Na+/Ca2+ exchangers in CRC tumorigenesis and progression. Understanding the detailed molecular mechanisms underlying the effects of [Ca2+] cyt on CRC is essential to develop Ca2+ channels/transporters as diagnostic and therapeutic targets. Targeting Ca2+ signaling for cancer therapy has become an emerging research area nowadays, although our knowledge about the roles of Ca2+ channels/transporters in tumorigenesis is still in the early stage, we still believe that they will act as novel preventive/therapeutic targets for CRC with potentially extensive clinical significance. [ABSTRACT FROM AUTHOR]