Amino acid-induced rapid gelation and mechanical reinforcement of hydrogels with low-hysteresis and self-recoverable and fatigue-resistant properties.

Hydrogels with rapid gelation ability and robust mechanical properties are highly desirable for nascent applications in biomedical, wearable electronic, industrial and agricultural fields. However, current rapid-gelation hydrogels are compromised by poor mechanical properties, complex design of precursor molecular structures and limited precursor species. Herein, we propose a facile and universal strategy to achieve rapid gelation, strengthening and toughening of free-radical polymerized hydrogels by introducing cheap and accessible amino acids. Amino acids not only activate persulfate to quickly produce free radicals and thus induce fast free radical polymerization, but also can form strong hydrogen bonds with the network chains to strengthen and toughen the hydrogels. For example, with the presence of L-serine, the acrylamide (AM) monomer shows rapid gelation within tens of seconds, and moreover the resulting hydrogel reaches a tensile strength of 0.45 MPa and a breaking strain of 2060%. More importantly, owing to the extremely dynamic feature of the hydrogen bonds between L-serine molecules and network chains, the hydrogel possesses the advantages of low hysteresis, rapid self-recovery capability and outstanding fatigue resistance. Furthermore, this strategy is general to a wide range of amino acids and monomers. We also demonstrate that this rapid, controllable and universal strategy for the fabrication of mechanically robust hydrogels holds tremendous potential for diverse practical applications, such as flexible electronic sensors and ultraviolet (UV)-blocking artificial skins.

Androgen increases klotho expression via the androgen receptor-mediated pathway to induce GCs apoptosis.

BACKGROUND: Many epidemiological studies have shown that anovulatory polycystic ovary syndrome (PCOS) is accompanied by hyperandrogenism. However, the exact mechanism of hyperandrogen-induced anovulation remains to be elucidated. In this study, we aimed to investigate the potential mechanism of anovulation in PCOS. To investigate the role of klotho as a key factor in the androgen receptor (AR)-mediated development of PCOS, we investigated the effects of testosterone on ovarian klotho expression in vivo and in vitro. RESULTS: Testosterone propionate (TP)-induced rats showed cycle irregularity, hyperandrogenism, polycystic ovarian changes, dyslipidemia. However, inhibition of AR expression could relieve PCOS traits. We also found that AR and klotho showed relatively high expression in PCOS rat ovarian tissue and in TP-induced granulosa cells (GCs), which was inhibited by the addition of flutamide. TP-induced GCs apoptosis was suppressed by AR antagonist, as well as silencing klotho expression in human GCs. Chromatin immunoprecipitation assay demonstrated that AR indirectly binds to the klotho promoter. CONCLUSIONS: Our results demonstrated TP mediates the expression of klotho via androgen receptor and klotho alterations could be a reason for ovarian dysfunction in PCOS.

A mechanically robust and stable estradiol-loaded PHEMA-based hydrogel barrier for intrauterine adhesion treatment.

Estrogen combined with physical barrier therapy may be a prospective method to repair a damaged endometrium and prevent postsurgical re-adhesion in the treatment of intrauterine adhesions (IUAs), but there lacks a suitable scaffold with good biocompatibility, appropriate mechanical properties, and drug-releasing kinetics. Herein, a mechanically robust and stable barrier based on the poly(hydroxyethyl methacrylate) (PHEMA) hydrogel combined with estradiol-loaded mesoporous silica is designed. The network is formed by covalent bonds and noncovalent coordination bonds, which endow the hydrogel with superior mechanical properties to most reported PHEMA-based hydrogels. Meanwhile, the covalent bonds impart excellent stability to the hydrogel, which maintains its structure and mechanical properties in a simulated uterine fluid for 30 days. The excellent mechanical properties and stability are comparable to those of a typical barrier material intrauterine device (IUD), enabling the hydrogel to be retained in the uterus and removed intact like an IUD. In vitro and in vivo experiments show that the hydrogel possesses good biocompatibility similar to pure PHEMA hydrogels. In addition, the hydrogel releases estradiol continuously and stably, and exhibits a good therapeutic effect in promoting the proliferation of endometrial cells and inhibiting the progression of fibrosis. Therefore, the combinational advantages make the present hydrogel very promising in IUA treatment.

Compliant, Tough, Anti-Fatigue, Self-Recovery, and Biocompatible PHEMA-Based Hydrogels for Breast Tissue Replacement Enabled by Hydrogen Bonding Enhancement and Suppressed Phase Separation.

Although hydrogel is a promising prosthesis implantation material for breast reconstruction, there is no suitable hydrogel with proper mechanical properties and good biocompatibility. Here, we report a series of compliant and tough poly (hydroxyethyl methacrylate) (PHEMA)-based hydrogels based on hydrogen bond-reinforcing interactions and phase separation inhibition by introducing maleic acid (MA) units. As a result, the tensile strength, fracture strain, tensile modulus, and toughness are up to 420 kPa, 293.4%, 770 kPa, and 0.86 MJ/m3, respectively. Moreover, the hydrogels possess good compliance, where the compression modulus is comparable to that of the silicone breast prosthesis (~23 kPa). Meanwhile, the hydrogels have an excellent self-recovery ability and fatigue resistance: the dissipative energy and elastic modulus recover almost completely after waiting for 2 min under cyclic compression, and the maximum strength remains essentially unchanged after 1000 cyclic compressions. More importantly, in vitro cellular experiments and in vivo animal experiments demonstrate that the hydrogels have good biocompatibility and stability. The biocompatible hydrogels with breast tissue-like mechanical properties hold great potential as an alternative implant material for reconstructing breasts.

Dendrobium nobile Lindl polysaccharides improve testicular spermatogenic function in streptozotocin-induced diabetic rats.

Dendrobium nobile Lindl polysaccharides (DNLP) exhibited various biological functions. This study aimed to investigate the protective effects of DNLP on testicular spermatogenic function in streptozotocin (STZ)-induced diabetic rats in comparison with metformin. The blood glucose level was significantly increased and the homeostatic model assessment for insulin resistance (HOMA-IR) aggravated markedly in diabetic rats. The weight of testis and epididymis, and the sperm number and motility were decreased in the diabetic rats. The pathologic changes occurred in the spermatogenic tubules along with the decreased number of spermatogenic cells, downregulated proliferating cell nuclear antigen (PCNA) and Sirtuin 1 (SIRT1) expression and increased cell apoptosis in the testes. Compared with the model group, DNLP and metformin treatment significantly decreased the level of blood glucose, improved the HOMA-IR, and increased the weight of testis and epididymis, as well as the sperm number and sperm motility. Furthermore, the pathologic changes in the spermatogenic tubules improved significantly with increased number of spermatogenic cells, the upregulation of PCNA and SIRT1 and suppression of cell apoptosis in the testes. Collectively, our study for the first time examined the effects of DNLP on the male reproductive system of STZ-induced diabetic rats, and indicated that DNLP was protective against diabetes mellitus-induced testis injury via increasing the proliferation, inhibiting cell apoptosis and upregulating SIRT1 expression in testicular spermatogenic cells.

The Role of the PI3K/AKT/mTOR Signalling Pathway in Male Reproduction.

Male fertility is closely related to the normal function of the hypothalamicpituitary- testicular axis. The testis is an important male reproductive organ that secretes androgen and produces sperm through spermatogenesis. Spermatogenesis refers to the process by which spermatogonial stem cells (SSCs) produce highly differentiated spermatozoa and is divided into three stages: mitosis, meiosis and spermiogenesis. Spermatogenesis requires SSCs to strike a proper balance between self-renewal and differentiation and the commitment of spermatocytes to meiosis, which involves many molecules and signalling pathways. Abnormal gene expression or signal transduction in the hypothalamus and pituitary, but particularly in the testis, may lead to spermatogenic disorders and male infertility. The phosphoinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signalling pathway is involved in many stages of male reproduction, including the regulation of the hypothalamus-pituitarygonad (HPG) axis during spermatogenesis, the proliferation and differentiation of spermatogonia and somatic cells, and the regulation of sperm autophagy and testicular endocrine function in the presence of environmental pollutants, particularly endocrinedisrupting chemicals (EDCs). In the PI3K/AKT/mTOR signalling pathway, mTOR is considered the central integrator of several signals, regulating metabolism, cell growth and proliferation. In particular, mTOR plays an important role in the maintenance and differentiation of SSCs, as well as in regulating the redox balance and metabolic activity of Sertoli cells, which play an important role in nutritional support during spermatogenesis.

Lycium barbarum Polysaccharides Improve Testicular Spermatogenic Function in Streptozotocin-Induced Diabetic Rats.

The objective of this study was to investigate the protective effects of Lycium barbarum polysaccharides (LBP) on testicular spermatogenic function in streptozotocin (STZ)-induced diabetic rats. Compared to the control group, blood glucose levels were significantly increased and the insulin resistance was markedly aggravated in STZ-induced diabetic rats. Further, the weight of testis and epididymis and the sperm number and motility were decreased in diabetic rats. Pathological changes were also observed in the spermatogenic tubules, along with a decreased number of spermatogenic cells, downregulated proliferating cell nuclear antigen (PCNA) expression, and increased cell apoptosis in the testes. Compared to the saline-treated diabetic rat group, metformin and LBP treatment significantly decreased the level of blood glucose and improved insulin resistance and testicular function. After treatment with metformin and LBP, the pathological changes in the spermatogenic tubules improved significantly, with an increase in the number of spermatogenic cells, upregulation of PCNA, and suppression of apoptosis in the testes. The expressions of sirtuin 1 (SIRT1) and hypoxia-inducible factor 1-alpha (HIF-1α) in diabetic testes were also upregulated by metformin or LBP treatment. In summary, LBP exerted protective effects by increasing cell proliferation, inhibiting cell apoptosis, and regulating SIRT1/HIF-1α expression in the testes of diabetic rats.

circFBXL5 promotes breast cancer progression by sponging miR-660.

Increasing studies have revealed that circular RNAs (circRNAs) play important roles in cancer progression. However, the potential involvement of circRNAs in breast cancer metastasis to lung is not clear so far. In this study, we conducted circular RNA microarrays of primary breast cancer tissues and lung metastatic tissues. The results revealed that circFBXL5 (hsa_circ_0125597) up-regulated the most in lung metastatic tissues. Survival analysis revealed that high levels of circFBXL5 correlated with worse outcome of breast cancer. Further experiments showed that knockdown of circFBXL5 inhibited breast cancer cell proliferation and migration to lung. Mechanism study showed that circFBXL5 acted as a sponge for miR-660 and compete binding to miR-660 with SRSF6, leading to increased expression of SRSF6. Collectively, our study highlighted the regulatory function of the circFBXL5/miR-660/SRSF6 pathway in breast cancer progression, which could be potential therapeutic targets for breast cancer.

Polycystic ovarian syndrome: Correlation between hyperandrogenism, insulin resistance and obesity.

Polycystic ovary syndrome (PCOS) is a complex and heterogeneous endocrine disease characterized by clinical or laboratorial hyperandrogenism, oligo-anovulation and metabolic abnormalities, including insulin resistance, excessive weight or obesity, type II diabetes, dyslipidemia and an increased risk of cardiovascular disease. The most significant clinical manifestation of PCOS is hyperandrogenism. Excess androgen profoundly affects granulosa cell function and follicular development via complex mechanisms that lead to obesity and insulin resistance. Most PCOS patients with hyperandrogenism have steroid secretion defects that result in abnormal folliculogenesis and failed dominant follicle selection. Hyperandrogenism induces obesity, hairy, acne, and androgenetic alopecia. These symptoms can bring great psychological stress to women. Drugs such as combined oral contraceptive pills, metformin, pioglitazone and low-dose spironolactone help improve pregnancy rates by decreasing androgen levels in vivo. Notably, PCOS is heterogeneous, and hyperandrogenism is not the only pathogenic factor. Obesity and insulin resistance aggravate the symptoms of hyperandrogenism, forming a vicious cycle that promotes PCOS development. Although numerous studies have been conducted, the definitive pathogenic mechanisms of PCOS remain uncertain. This review summarizes and discusses previous and recent findings regarding the relationship between hyperandrogenism, insulin resistance, obesity and PCOS.

The Effects of Cholesterol Metabolism on Follicular Development and Ovarian Function.

Cholesterol is an important substrate for the synthesis of ovarian sex hormones and has an important influence on follicular development. The cholesterol in follicular fluid is mainly derived from plasma. High-density lipoprotein (HDL) and lowdensity lipoprotein (LDL) play important roles in ovarian cholesterol transport. The knockout of related receptors in the mammalian HDL and LDL pathways results in the reduction or absence of fertility, leading us to support the importance of cholesterol homeostasis in the ovary. However, little is known about ovarian cholesterol metabolism and the complex regulation of its homeostasis. Here, we reviewed the cholesterol metabolism in the ovary and speculated that regardless of the functioning of cholesterol metabolism in the system or the ovarian microenvironment, an imbalance in cholesterol homeostasis is likely to have an adverse effect on ovarian structure and function.

Dyslipidemia involvement in the development of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is widely accepted as the most common endocrine abnormality in women of childbearing age and may be accompanied by dyslipidemia, hyperandrogenism, hyperinsulinemia, oxidative stress and infertility. Dyslipidemia is now known to play an important role in the development of PCOS. Lipid abnormalities, including elevated low-density lipoprotein and triglyceride levels and reduced high-density lipoprotein levels, are often found in women with PCOS and play an important role in PCOS; therefore, we summarize the effect of lipid abnormalities on hyperandrogenism, insulin resistance, oxidative stress and infertility in PCOS and review the effects of common lipid-lowering drugs on patients with PCOS. The purpose of this article is to elucidate the mechanisms of lipid metabolism abnormalities in the development of PCOS.

The roles of retinoic acid in the differentiation of spermatogonia and spermatogenic disorders.

Male fertility depends on the regulatory balance between germ cell self-renewal and differentiation, and the spatial and temporal patterns of this balance must be maintained throughout the life cycle. Retinoic acid and its receptors are important factors in spermatogenesis. Spermatogonia cells can self-proliferate and differentiate and have unique meiotic capabilities; they halve their genetic material and produce monomorphic sperm to pass genetic material to the next generation. A number of studies have found that the spermatogenesis process is halted in animals with vitamin A deficiency and that most germ cells are degraded, but they tend to recover after treatment with RA or vitamin A. This literature review discusses our understanding of how RA regulates sperm cell differentiation and meiosis and also reviews the functional information and details of RA.

Nogo­B receptor in relevant carcinoma: Current achievements, challenges and aims (Review).

The novel neurite outgrowth inhibitor B (Nogo­B) receptor (NgBR) is specific for Nogo­B, which is highly expressed in various human organs and cells, including the lung, liver, kidney, smooth muscle cells, blood vessel endothelial cells and inflammatory cells. Previous studies have indicated that NgBR directly interacts with Nogo­B and is able to independently influence lipid and cholesterol homeostasis, angiogenesis, N­glycosylation, the epithelial-mesenchymal transition, the chemotaxis of endothelial cells and cellular proliferation and apoptosis. These multiple functions and actions of this receptor provide an understanding of the important roles of NgBR in various conditions, including fatty liver, atherosclerosis, intracranial microaneurysms, retinitis pigmentosa and severe neurological impairment. Furthermore, NgBR has been demonstrated to exert protean, multifunctional and enigmatic effects in cancer. The present review summarizes the latest knowledge on the suppressing and activating effects of NgBR, emphasizing its function in cancer. Further basic and medical research on this receptor may provide novel insight into its clinical implications on the prognosis of relevant human cancer types.

Characterization of cholesterol metabolism in Sertoli cells and spermatogenesis (Review).

The Sertoli cell, which is the supporting cell of spermatogenesis, has an important role in the endocrine and paracrine control of spermatogenesis. Functionally, it provides the cells of the seminiferous epithelium with nutrition, conveys mature spermatids to the lumen of seminiferous tubules, secretes androgen­binding protein and interacts with endocrine Leydig cells. In addition, the levels of cholesterol, as well as its intermediates, vary greatly between nongonadal tissues and the male reproductive system. Throughout spermatogenesis, a dynamic and constant alteration in the membrane lipid composition of Sertoli cells occurs. In several mammalian species, testis meiosis­activating sterol and desmosterol, as well as other cholesterol precursors, accumulate in the testes and spermatozoa. In addition, certain cholesterogenic genes exhibit stage­specific expression patterns during spermatogenesis, including the cytochrome P450 enzyme lanosterol 14α­demethylase. Inconsistency in the patterns of gene expression during spermatogenesis indicates a cell­type specific and complex temporary modulation of lipids and cholesterol, which also implicates the dynamic interactions between Sertoli cells and germ cells. Furthermore, in the female reproductive tract and during epididymal transit, which is a prerequisite for valid fertilization, the modulation of cholesterol occurring in spermatozoal membranes further indicates the functional importance of sterol compounds in spermatogenesis. However, the exact role of cholesterol metabolism in Sertoli cells in sperm production is unknown. The present review article describes the progress made in the research regarding the characteristics of the Sertoli cell, particularly the regulation of its cholesterol metabolism during spermatogenesis.

Neurite Outgrowth Inhibitor B Receptor: A Versatile Receptor with Multiple Functions and Actions.

Members of the reticulon protein family are predominantly distributed within the endoplasmic reticulum. The neurite outgrowth inhibitor (Nogo) has three subtypes, including Nogo-A (200 kDa), Nogo-B (55 kDa), and Nogo-C (25 kDa). Nogo-A and Nogo-C are potent Nogos that are predominantly expressed in the central nervous system. Nogo-B, the splice variant of reticulon-4, is expressed widely in multiple human organ systems, including the liver, lung, kidney, blood vessels, and inflammatory cells. Moreover, the Nogo-B receptor (NgBR) can interact with Nogo-B and can independently affect nervous system regeneration, the chemotaxis of endothelial cells, proliferation, and apoptosis. In recent years, it has been demonstrated that NgBR plays an important role in human pathophysiological processes, including lipid metabolism, angiogenesis, N-glycosylation, cell apoptosis, chemoresistance in human hepatocellular carcinoma, and epithelial-mesenchymal transition. The pathophysiologic effects of NgBR have garnered increased attention, and the detection and enhancement of NgBR expression may be a novel approach to monitor the development and to improve the prognosis of relevant human clinical diseases.

Identification and analysis of the promoter region of the STGC3 gene.

INTRODUCTION: Nasopharyngeal carcinoma (NPC) is a common malignant tumor of the head and neck. The STGC3 gene is related to development of nasopharyngeal cancer. The aim of this study is to explore the promoter region of the STGC3 gene. MATERIAL AND METHODS: The bioinformatic technique was applied to predict its promoter region and construct the gene promoter region luciferase for the gene vector and transfection of the human embryonic kidney epithelial 293T cell line, human nasopharyngeal carcinoma CNE2 cell line and immortalized nasopharyngeal epithelial NP69 cell line. The recombinant plasmid pGL3-en283, pGL3-en281, pGL3-en571, empty plasmid pGL3-control, negative control pGL3-enhance and internal control of marine intestine luciferase expression vector pRL-SV40 were transfected into NP69 cells, 293T cells and CNE2 cells. Dual luciferase activity detection showed luciferase luminescence values and marine intestine luciferase luminescence values. Relative luciferase activity (RLA) in each cell was calculated. RESULTS: We observed strong promoter activity of plasmid pGL3-en283, pGL3-en281 and pGL3-en571 in NP69, 293T and CNE2 cells compared with the negative control pGL3-enhance plasmid. Among them, pGL3-en281 showed the strongest promoter activity, and these three kinds of recombinant plasmids showed stronger promoter activity in 293T cells than in CNE2 cells. CONCLUSIONS: The pGL3-en281 plasmid showed stronger promoter activity than pGL3-en571 in the three cells, indicating that -11048 bp to -653 bp might be the core promoter region.

[Effect of PFT-α on apoptosis of spermatogenic cells caused by enorchia].

OBJECTIVE: To determine the molecular mechanism of germ cell apoptosis via investigating the effect of PFT-α on the expression of p53 and bcl-2/bax during experimental cryptorchid cell apoptosis. METHODS: Male Sprague-Dawley rats were assigned into 4 groups: a sham-operated group, a cryptorchid group, a cryptorchid+p53 inhibitor (p53 inhibitor-alpha, PFT-α) group, and a cryptorchid+dissolvent of PFT-α [dimethyl sulphoxide (DMSO)] group. Unilateral cryptorchidism was surgically induced in the rats of the cryptorchid group, PFT-α group, and cryptorchid+dissolvent of PFT-α group. The rats in the PFT-α group and cryptorchid+dissolvent of PFT-α group were intra-peritoneally injected PFT-α and dissolvent of PFT-α, respectively, once a day. The rats were killed on the 7th day after the surgery. The morphology of spermatogenic epithelium at the side of surgery in the rats was observed under light microscope. The apoptosis of spermatogenic cells in the unilateral cryptorchidism was evaluated by TUNEL and flow cytometry (FCM). The protein expression levels of p53, bcl-2, and Bax were detected by Western blot and immunohistochemical assay in turn. RESULTS: Compared with the cryptorchid groups and the cryptorchid+dissolvent of PFT-α group, the seminiferous epithelium of the cryptorchid+p53 inhibitor group appeared orderly, with thicker cell layers and lower apoptosis index, weak protein expression level of p53/Bax and strong protein expression level of bcl-2. CONCLUSION: PFT-α inhibits the germ cell apoptosis caused by the experimental cryptorchidism via increasing the expression of bcl-2 and decreasing the expression of p53 and bax.

MicroRNA-124 inhibits proliferation and induces apoptosis by directly repressing EZH2 in gastric cancer.

MicroRNA-124 (miR-124), a pivotal member of the p53 network, was found to be down-regulated in multiple types of tumors and further reported as tumor suppressor microRNA. In this study, we found that miR-124 was down-regulated in gastric cancer cell lines and specimens. Restoration of miR-124 expression inhibited the proliferation and colony formation of gastric cancer cells. EZH2 (enhancer of zeste homolog 2), which has been shown to be an important transcription factor involved in the proliferation and metastasis of tumor cells, was here confirmed to be a direct target gene of miR-124. On the other hand, silencing EZH2 also inhibits cell proliferation of gastric cancer cells. Furthermore, the treatment combining miR-124 with 5-fluorouracil (5-FU) significantly showed more efficient anti-tumor effects than single treatment of miR-124 or 5-FU, and over-expression of miR-124 suppresses the tumor growth in vivo. Our study indicate that miR-124 can suppress gastric cancer cell growth by directly targeting the EZH2 gene and sensitize the treatment effect of 5-FU. Therefore, miR-124 shows tumor-suppressive activity and may be a new and useful approach of gastric cancer therapy.

The 656C and 725C are two important sites in gene STGC3 for its negative regulation on cell growth.

The aim of this study was to analyze the functional sites of the nasopharyngeal candidate tumour suppressor gene STGC3. Recombinant plasmid pcDNA3.1TM/myc-His B-STGC3 was constructed. Site-directed mutagenesis of pcDNA3.1TM/myc-His B-STGC3 plasmid at sites of C656G, C725T and T913G was induced by the Stratagene mutagenesis method. Recombinant plasmids with point mutations at C656G, C725T and T913G of gene STGC3 were named as STGC3-C656G, STGC3-C725T and STGC3-T913G, respectively. CNE2 cell lines stably expressing wild and mutant STGC3 genes were established. STGC3 expression was detected by Western Blotting and immunocytochemistry. Cell proliferation was analyzed by 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and trypan blue staining. Flow cytometry analysis was used to assess apoptosis of CNE2 cells. Bax protein expression was detected by Western Blotting. Proteins of wild-type and mutant STGC3 genes were expressed in the cytoplasm and nucleus of CNE2 cells. Compared with the control groups, in cells stably expressing wild-type STGC3 and STGC3-T913G genes, cell proliferation was significantly inhibited, whereas levels of apoptosis and Bax protein expression were significantly increased. However, the cell proliferation, apoptosis and Bax protein expression in cells stably expressing STGC3-C656G and STGC3-C725T genes were not significantly different from those in the control groups. Our results suggest that mutations at 656C and 725C, but not 913T, abolished the effects of the wild-type STGC3 gene on CNE2 cells and that the 656C and 725C were important sites in gene STGC3 for its negative regulation on cell growth.

Involvement of EBV-encoded BART-miRNAs and dysregulated cellular miRNAs in nasopharyngeal carcinoma genesis.

The definite molecular mechanisms underlying the genesis of nasopharyngeal carcinomas (NPCs) remain to be completely elucidated. miRNAs are small non-coding RNAs which are implicated in cell proliferation, apoptosis, and even carcinogenesis through negatively regulating gene expression post-transcriptionally. EBV was the first human virus found to express miRNAs. EBV-encoded BART-miRNAs and dysregulated cellular miRNAs are involved in carcinogenesis of NPC by interfering in the expression of viral and host cell genes related to immune responses and perturbing signal pathways of proliferation, apoptosis, invasion, metastasis and even radio-chemo-therapy sensitivity. Additional studies on the roles of EBV-encoded miRNAs and cellular miRNAs will provide new insights concerning the complicated gene regulated network and shed light on novel strategies for the diagnosis, therapy and prognosis of NPC.