Multiple myeloma (MM) is a malignant disease of plasma cells with complex pathology, causing significant morbidity due to its end-organ destruction. The outcomes of patients with myeloma have significantly improved in the past couple of decades with the introduction of novel agents, such as proteasome inhibitors, immunomodulators, and monoclonal antibodies. However, MM remains incurable and presents considerable individual heterogeneity. MicroRNAs (miRNAs) are short, endogenous noncoding RNAs of 19–22 nucleotides that regulate gene expression at the posttranscriptional level. Numerous studies have shown that miRNA deregulation is closely related to MM pathology, including tumor initiation, progression, metastasis, prognosis, and drug response, which make the complicated miRNA network an attractive and marvelous area of investigation for novel anti-MM therapeutic approaches. Herein, we mainly summarized the current knowledge on the roles of miRNAs, which are of great significance in regulating pathological factors involved in MM progressions, such as bone marrow microenvironment, methylation, immune regulation, genomic instability, and drug resistance. Meanwhile, their potential as novel prognostic biomarkers and therapeutic targets was also discussed.

The immune system in patients with cancer often fails to control tumour growth because of deficient immunogenicity of tumour cells. Ganoderma lucidum polysaccharides (Gl-PS) are believed to have anti-tumour effects by boosting host immune function. Additionally, Gl-PS may have some direct effects on tumour cells in the activation of lymphocytes, thus enhancing the immunogenicity of tumour cells. We tested the effects of Gl-PS in lymphocyte activation by incubating Gl-PS with a tumour cell line deficient in antigen presentation. Our study showed that Gl-PS can promote B16F10 melanoma cells to induce lymphocyte proliferation, CD69 and FasL expression and IFN-c production, indicating that Gl-PS can improve the nature of B16F10 cells to activate lymphocytes. Furthermore, H-2D b [a major histocompatibility (MHC) class I molecule], and B7-1 and B7-2 (two prominent co-stimulatory molecules expressed on B16F10 cells) were enhanced by Gl-PS, suggesting that these molecules may at least partially be involved in the process of Gl-PS on B16F10 cells to activate lymphocytes.The concept of immunosurveillance was first presented in 1957 and supported by the evidence of tumour-specific antigens [1]. However, the immune system in patients with cancer often fails to control tumour growth because of deficient immunogenicity of the tumour cells. Tumour cells use various strategies to evade the recognition by the host immune system. Mechanisms, such as MHC class I down-regulation, antigen loss, antigen modulation or the expression of inhibitory molecules, may explain the failure of an endogenous immune response in tumour control [2]. A major goal of immunotherapy is to generate an effective cell-mediated immune response with active or adoptive immunotherapy. It is clearly important to enhance immunogenicity of malignant tumour cells for induction of anti-tumour responses; however, attempts to activate a specific immune response against malignancies have been tried with only limited success.Ganoderma lucidum (Gl) has been widely used in China for centuries to promote longevity and improve vigour without appreciable adverse effects [3]. Ganoderma lucidum polysaccharides (Gl-PS), extracts from Gl, have multiple biological activities. Over the past two decades, numerous studies have demonstrated the immunomodulatory and antitumour activities of Gl-PS [4-6]. The anti-tumour effect of Gl-PS is believed to be mediated primarily by immune mechanisms. Gl-PS can increase cytokine production, improve dendritic cell maturation and function [7], improve cytokine-induced killer cell (CIK) function [5], improve cytotoxic T lymphocytes (CTL) function [8], and inhibit the growth of vascular endothelial cell and the induction of vascular endothelial growth factor (VEGF) in human lung cancer cell [9]. Gl-PS can also enhance the function of immunological effector cells in immunosuppressed mice [10]. In addition, recent research has shown that Gl-PS can reverse multidrug resistance (MDR) by down-regulating the expression of MDR-1 and MDR-assoc...

B16F10-CS suppressed lymphocyte proliferation and perforin and granzyme B production in lymphocytes after induction with phytohemagglutinin, as well as lymphocyte proliferation in the mixed lymphocyte reaction. This suppression may be associated with elevated levels of immunosuppressive IL-10, TGF-β1 and VEGF in B16F10-CS. Gl-PS had antagonistic effects on the immunosuppression induced by B16F10-CS, suggesting the potential for Gl-PS in cancer immunotherapy.

The aim of the current study was to investigate the regulatory effect of sericin on the hepatic insulin-phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in a type 2 diabetes rat model. Male Sprague Dawley rats were randomly divided into four groups: Control group, diabetic model group, high-dose sericin group and low-dose sericin group, with 12 rats in each group. Fasting blood glucose was detected by the glucose oxidase method, and hepatic glycogen was determined by periodic acid-Schiff staining. The morphology of the liver was observed by hematoxylin and eosin staining. Immunohistochemical staining, western blotting and reverse transcription-quantitative polymerase chain reaction were used to determine the protein and mRNA expression levels of insulin receptor (IR), IR substrate-1 (IRS-1), PI3K and AKT. Compared with the control group, the blood glucose of the diabetic model group was significantly increased (P<0.05). The glycogen content and the expression levels of IR, IRS-1, PI3K and AKT in the diabetic model group were significantly lower (P<0.05), and the liver morphological structure of the diabetic model group exhibited obvious pathological changes compared with the control group. Compared with the diabetic model group, the blood glucose of the high- and low-dose sericin groups was significantly reduced, while the glycogen content and the expression levels of IR, IRS-1, PI3K and AKT in the sericin treatment groups were significantly increased (P<0.05). Additionally, the liver pathological changes of high-dose and low-dose sericin groups were markedly reduced. Sericin may enhance the signaling transduction effect of insulin by upregulating the expression levels of key factors (IR, IRS-1, PI3K and AKT) in the liver insulin-PI3K/AKT signaling pathway, thus promoting glucose transport and liver glycogen synthesis, and further reducing blood glucose.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This study aimed to investigate the correlations of long non-coding RNA maternally expressed gene 3 (lnc-MEG3), microRNA (miR)-21, and lnc-MEG3/miR-21 axis with disease risk, inflammation, disease severity, and 28-day mortality of sepsis. Methods: Totally, 219 sepsis patients and 219 health controls (HCs) were enrolled. Plasma samples were obtained from sepsis patients within 24 hours after admission and from HCs on enrollment to detect lnc-MEG3 and miR-21 expressions by realtime quantitative polymerase chain reaction. Results: The lnc-MEG3 expression and lnc-MEG3/miR-21 axis were increased, while miR-21 expression was decreased in sepsis patients compared with HCs. Lnc-MEG3 (area under the curve (AUC): 0.887, 95% confidence interval (CI): 0.856-0.917) andlnc-MEG3/miR-21 axis (AUC: 0.934, 95% CI: 0.909-0.958) had good values for predicting elevated sepsis risk, while miR-21 (AUC: 0.801, 95% CI: 0.758-0.844) presented a good predictive value for reduced sepsis risk. Furthermore, lnc-MEG3 expression and lnc-MEG3/miR-21 axis positively correlated with, whereas miR-21 expression negatively correlated with acute pathologic and chronic health evaluation II, sequential organ failure assessment score, serum creatinine, C-reactive protein, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-17 in sepsis patients. Additionally, lnc-MEG3 (AUC: 0.704, 95% CI: 0.626-0.783) and lnc-MEG3/miR-21 axis (AUC: 0.669, 95% CI: 0.589-0.750) exhibited acceptable values in predicting higher 28-day mortality risk, while miR-21 (AUC: 0.588, 95% CI: 0.505-0.672) presented a poor predictive value for lower 28-day mortality risk in sepsis patients. Conclusion:Lnc-MEG3 might serve as a potential biomarker for the development, progression, and prognosis prediction of sepsis via interacting with miR-21.