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The application of iron-bridged polyoxometalates has firstly been studied. We propose a new molecule-to-particle synthetic strategy to synthesize a family of bimetallic composites as NRR catalysts with excellent stability and reproducibility.

Polychlorinated biphenyl (PCB)-degrading strains resuscitated by resuscitation promoting factor (Rpf) enlarged pure degraders to screen effective bio-inoculants for soil bioaugmentation. In this study, whole-genome analysis and PCB-degrading performance of a resuscitated strain LS1 were investigated. Importantly, the persistence and the physiological response of soil-inoculated LS1 were checked. The results indicate that the Bacillus sp. strain LS1 possessed the potential to degrade polycyclic aromatic compounds. LS1 exhibited better performance in degrading PCBs 18 and 52, but lower PCB 77 degradation capability. At PCBs concentration of 10 mg/L, the degradation efficiencies of PCBs 18, 52 and 77 within 96 h were 62.8 %, 59.6 % and 39.8 %, respectively. Combined the bph genes and metabolites detected, as well as the genes found in the genome, the abilities of LS1 for oxidative dehalogenation and mineralization of PCBs via HOPDA-benzoate-protocatechuate-β-ketoadipate pathway were determined. Notably, LS1 can still maintain survival and culturable state after inoculation into PCB-contaminated soil for 70 days. This is the first report to demonstrate the fate of resuscitated strain when used as soil bio-inoculant, which revealed the necessity and feasibility of using resuscitated strains to enhance bioremediation of PCB-contaminated soils.

The mellow and thick taste is a unique characteristic of pu−erh ripe tea infusion, and it is closely related to the chemical composition of pu−erh ripe tea, which is less studied. This paper clarifies and compares the chemical composition of pu−erh ripe tea to that of the raw materials of sun−dried green tea, and uses membrane separation technology to separate pu−erh ripe tea into the rejection liquid and the filtration liquid. The results show that microorganisms transformed most physicochemical components, except caffeine, during the pile fermentation. It was found that total tea polyphenols, soluble proteins, total soluble sugars, theabrownin, and galloylated catechins became enriched in the rejection liquid, and the rejection liquid showed a more obvious mellow and thick characteristic. Taste interactions between crude protein, crude polysaccharide, and theabrownin were determined. They illustrated that the mellow and thick taste of pu−erh ripe tea with the addition of theabrownin increased from 4.45 to 5.13. It is of great significance to explore the chemical basis of the mellow and thick taste in pu−erh tea for guiding the pu−erh tea production process and for improving the quality of pu−erh tea.

Background: Triple-negative breast cancer (TNBC) is a great threat to global women's health due to its high metastatic potential. Epithelial-to-mesenchymal transition (EMT) is considered as a key event in the process of metastasis. So the pharmacological targeting of EMT might be a promising strategy in improving the therapeutic efficacy of TNBC. Here, we investigated the effect of shikonin exerting on EMT and consequently the metastasis of TNBC cells and its underlying mechanism. Methods: The invasive and migratory capacities of MDA-MB-231 and BT549 cells were tested using transwell invasion and wound healing assay. MiR-17-5p expression was examined by qRT-PCR. MiR-17-5p targeted genes were predicted with different bioinformatic algorithms from four databases (TargetScan, miRanda, PITA and picTar) and further screened by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The differential expressions of predicted genes and their correlations with miR-17-5p were identified in breast cancer patients based on The Cancer Genome Atlas (TCGA) database. The interaction between phosphatase and tensin homolog deleted on chromosome ten (PTEN) and miR-17-5p was analyzed by luciferase reporter assay. The overexpression vector and small interfering RNA were constructed to investigate the role PTEN played in metastasis and EMT regulation. The expressions of EMT markers, protein kinase B (Akt) and phospho-Akt (p-Akt) were evaluated by western blot. Results: Shikonin suppressed the migration and invasion of MDA-MB-231 and BT549 cells and meanwhile the corresponding alterations of EMT biomarkers were observed in shikonin treated MDA-MB-231 cells. Shikonin inhibited the expression of miR-17-5p, which was upregulated in breast cancer. The 3'-untranslated region (3'-UTR) of PTEN was found to be direct binding target of miR-17-5p by luciferase reporter assays. PTEN functioned as a suppressor both in the metastasis and EMT of TNBC cells. Moreover, Akt and p-Akt (Ser473) were involved in the process of inhibition in cancer cell migration, invasion and EMT by shikonin. Conclusions: Shikonin inhibits migration and invasion of TNBC cells by suppressing EMT via miR-17-5p/PTEN/Akt pathway. This suggests shikonin as a promising therapeutic agent to counteract metastasis in the TNBC patients.

Most functional microorganisms cannot be cultivated due to entering a viable but non-culturable (VBNC) state, which limits the characterization and application of polychlorinated biphenyl (PCB)-degrading strains. Resuscitating VBNC bacteria could provide huge candidates for obtaining high-efficient PCB degraders. However, limited studies have focused on the ability of resuscitated strains for PCBs degradation. In the present study, whole-genome analysis of a resuscitated strain SPC0, and its performances in degradation of three prevalent PCB congeners (PCBs 18, 52 and 77) were investigated. The results indicate that the strain SPC0 belonged to the genus Streptococcus, possessed the degradation potential for aromatic xenobiotics. The SPC0 could effectively degrade PCBs 18 and 52, but exhibited lower degradation efficiency of PCB 77. Degradation of PCBs 18 and 52 could be fitted well by zero-order model, whereas the fittest model for PCB 77 degradation was pseudo second-order kinetics. The bph genes expression, chloride ions release and degradation metabolites identification, suggest that SPC0 possessed the capability of oxidative dehalogenation and mineralization of PCBs. Interestingly, SPC0 can degrade PCBs via the bph-encoded biphenyl pathway, and further mineralize metabolite dichlorobenzoate via protocatechuate pathway. This study is the first to show that a strain belonging to genus Streptococcus possessed PCB-degrading capability, which uncovered the powerful potential of resuscitated strains for bioremediation of PCB-contaminated sites.

Cytology and histology obstacles have been the main barriers to multiple tissues injury repair. In search of the most promising treatment strategies for spinal cord injury (SCI), stem cell-based transplantation coupled with various materials/technologies have been explored extensively to enhance SCI repair. Chitosan (CS) has demonstrated immense potential for widespread application in the form of scaffolds and micro-particles for SCI repair. The current review summarizes the evidences for stem cell-based transplantation and CS in SCI repair. Stem cells transplantation, which plays a key role in the repair of SCI, mainly results from its neural differentiation potential and neurotrophic effects. Application of CS enhances the survival of grafted stem cells, upregulates the expression level of neurotrophic factors and heightens the neural differentiation of stem cells as well as the functional recovery of spinal cord. Meanwhile, CS can also be exploited as growth factors/RNA carriers to control the release of regenerating molecules which are beneficial to damage spinal cord repair.

Accuracy and efficiency are essential topics in the current biometric feature recognition and security research. This paper proposes a deep neural network using bidirectional feature extraction and transfer learning to improve finger-vein recognition performance. Above all, we make a new finger-vein database with the opposite position information of the original one and adopt transfer learning to make the network suitable for our overall recognition framework. Next, the feature extractor is constructed by adjusting the unidirectional database’s parameters, capturing vein features from top to bottom and vice versa. Correspondingly, we concatenate the above two features to form the finger-veins’ bidirectional features, which are trained and classified by Support Vector Machines (SVM) to realize recognition. Experiments are conducted on the Malaysian Polytechnic University’s published database (FV-USM) and finger veins of Signal and Information Processing Laboratory (FV-SIPL). The accuracy of our proposed algorithm reaches 99.67% and 99.31%, which is significantly higher than the unidirectional recognition under each database. Compared with the algorithms cited in this paper, our proposed model based on bidirectional feature enjoys higher accuracy, faster recognition speed than the state-of-the-art frameworks, and excellent practical value.

Exosomes are small extracellular vesicles (EVs) secreted by almost all cells, which have been recognized as a novel platform for intercellular communication in the central nervous system (CNS). Exosomes are capable of transferring proteins, nucleic acids, lipids, and metabolites between neurons and glial cells, contributing to CNS development and maintenance of homeostasis. Evidence shows that exosomes originating from CNS cells act as suppressors or promoters in the initiation and progression of neurological disorders. Moreover, these exosomes have been shown to transfer molecules associated with diseases through the blood-brain barrier (BBB) and thus can be detected in blood. This unique feature enables exosomes to act as potential diagnostic biomarkers for neurological disorders. In addition, a substantial number of researches have indicated that exosomes derived from mesenchymal stem cells (MSCs) have repair effects on neurological disorders. Herein, we briefly introduce the roles of exosomes under physiological and pathological conditions. In particular, novel roles of exosomes as potential diagnostic biomarkers and therapeutic tools for neurological disorders are highlighted.

Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) are nano-sized membrane-bound vesicles that have been reported to facilitate skin regeneration and repair. However, the roles played by hucMSC-ex in ultraviolet (UV) radiation-induced skin photodamage and the underlying mechanisms remain unknown. To investigate the functions of hucMSC-ex in a rat model of acute skin photodamage, immunofluorescence and immunohistochemical staining, quantitative real-time-polymerase chain reaction (qRT-PCR), western blot, and gene silencing assays were performed. We found that the in vivo subcutaneous injection of hucMSC-ex elicited antioxidant and anti-inflammatory effects against UV radiation-induced DNA damage and apoptosis. Further studies showed that the sirtuin 1 (SIRT1) expression level in skin keratinocytes (HaCaT) decreased in a time- and dose-dependent manner under in vitro UV radiation induced-oxidative stress conditions, which could be reversed by treatment with hucMSC-ex. The activation of SIRT1 significantly attenuated UV- and H2O2-induced cytotoxic damage by inhibiting oxidative stress and promoting the activation of autophagy. Our study found that 14-3-3ζ protein, which was delivered by hucMSC-ex, exerted a cytoprotective function via the modulation of a SIRT1-dependent antioxidant pathway. Collectively, our findings indicated that hucMSC-ex might represent a new potential agent for preventing or treating UV radiation-induced skin photodamage and aging.

The electrocatalytic nitrogen reduction reaction (NRR) is known as a promising mean of nitrogen fixation to mitigate the energy crisis and facilitate fertilizer production under mild circumstances. For electrocatalytic reactions, the design of efficient catalysts is conducive to reducing activation energy and accelerating lethargic dynamics. Among them, hollow structural materials possess cavities in their structures, which can slack off the escape rate of N2 and reaction intermediates, prolong the residence time of N2, enrich the reaction intermediates’ concentration, and shorten electron transportation path, thereby further enhancing their NRR activity. Here, the basic synthetic strategies of hollow structural materials are introduced first. Then, the recent breakthroughs in hollow structural materials as NRR catalysts are reviewed from the perspective of intrinsic, mesoscopic, and microscopic regulations, aiming to discuss how structures affect and improve the catalytic performance. Finally, the future research directions of hollow structural materials as NRR catalysts are discussed. This review is expected to provide an outlook for optimizing hollow structural NRR catalysts., Recent progresses about the advantages of hollow structural materials for nitrogen reduction reaction are summarized. Besides, the top‐down fine regulating strategies from the perspective of intrinsic, mesoscopic, and microscopic regulations are introduced, aiming to discuss how various structures affect and improve the catalytic performance. These outputs render hollow structural materials to be the centerpiece for various applications, especially energy conversion applications.

Human umbilical cord mesenchymal stem cell-derived exosomes (HucMSC-Ex) are a promising tool for the repair of acute kidney injury (AKI) caused by cisplatin and ischemia/reperfusion. However, the roles of hucMSC-Ex in sepsis-associated AKI repair and its mechanism are largely unknown. Hence, we constructed a sepsis model through cecal ligation and puncture (CLP), testing the benefits of hucMSC-Ex in the sepsis in terms of survival rate, serum renal markers levels, morphological changes and apoptosis. Immunohistochemistry staining and immunofluorescence assay were used to investigate the role of NF-κB activity in the repair of sepsis-associated AKI with hucMSC-Ex. HK-2 cells were transfected with microRNA-146b (miR-146b) mimics and inhibitors, respectively, and the regulatory effect of miR-146b on NF-κB activity was studied. We found that hucMSC-Ex treatment significantly decreased the serum creatinine (Cr) and blood urea nitrogen (BUN) levels, ameliorated the morphological damage and inhibited renal tubular cells apoptosis. More importantly, the survival rate at 72 h was 28% in CLP group and 45% in hucMSC-Ex group, respectively. Treatment with hucMSC-Ex improved survival in mice with sepsis. These effects of hucMSC-Ex were mediated by the inhibition of NF-κB activity and the lessening of pro-inflammatory response. Furthermore, hucMSC-Ex significantly increased miR-146b expression in kidney tissues. Conversely, interleukin (IL)-1 receptor-associated kinase (IRAK1) level, which is the target gene of miR-146b, clearly decreased in hucMSC-Ex group. In brief, this study showed that treatment with hucMSC-Ex decreased IRAK1 expression through the up-regulation of miR-146b level, led to the inhibition of NF-κB activity, and eventually alleviated sepsis-associated AKI and improved survival in mice with sepsis. HucMSC-Ex may be a novel therapeutic agent for the reduction of sepsis-associated AKI.

Luteolin has been reported to attenuate ischemia/reperfusion (I/R) injury in the diabetic heart through endothelial nitric oxide synthase- (eNOS-) related antioxidative response. Though the nuclear factor erythroid 2-related factor 2 (Nrf2) is regarded as a key endogenous factor to reduce diabetic oxidative stress, whether luteolin reduces cardiac I/R injury in the diabetic heart via enhancing Nrf2 function needs to be clarified. We hypothesized that pretreatment with luteolin could alleviate cardiac I/R injury in the diabetic heart by affecting the eNOS/Nrf2 signaling pathway. The diabetic rat was produced by a single injection of streptozotocin (65 mg/kg, i.p.) for 6 weeks, and then, luteolin (100 mg/kg/day, i.g.), eNOS inhibitor L-NAME, or Nrf2 inhibitor brusatol was administered for the succedent 2 weeks. After that, the isolated rat heart was exposed to 30 min of global ischemia and 120 min of reperfusion to establish I/R injury. Luteolin markedly ameliorated cardiac function and myocardial viability; upregulated expressions of heme oxygenase-1, superoxide dismutase, glutathione peroxidase, and catalase; and reduced myocardial lactate dehydrogenase release, malondialdehyde, and 8-hydroxydeoxyguanosine in the diabetic I/R heart. All these ameliorating effects of luteolin were significantly reversed by L-NAME or brusatol. Luteolin also markedly reduced S-nitrosylation of Kelch-like ECH-associated protein 1 (Keap1) and upregulated Nrf2 and its transcriptional activity. This effect of luteolin on Keap1/Nrf2 signaling was attenuated by L-NAME. These data reveal that luteolin protects the diabetic heart against I/R injury by enhancing eNOS-mediated S-nitrosylation of Keap1, with subsequent upregulation of Nrf2 and the Nrf2-related antioxidative signaling pathway.

With the development of wearable sensing technology, increasing attention has been given to flexible wearable sensors with textile structures. With a change in the coil structure, conductive knitted fabric can show satisfactory strain sensing performance and can be used to monitor human activities and physical signs. In this paper, polyaniline (PANI)/cotton conductive knitted fabric was prepared via the deposition of a PANI conductive layer on the fabric surface via in situ polymerization of aniline. The surface morphology, chemical structure, electrical conductivity and mechanical properties of the conductive knitted fabric were investigated, and a flexible fabric strain sensor was fabricated with the conductive knitted fabric as a sensing element. In addition, the sensor is applied to monitor the state of human activity/signs. The results demonstrate that the resistivity of the conductive knitted fabric is reduced by more than 8 orders of magnitude compared with the untreated cotton fabric to 0.275 × 103 Ω cm The conductive knitted fabric shows satisfactory strain sensing performance with high linearity and a maximum gauge factor of more than 30. The strain influences the sensing repeatability of conductive knitted fabric. If the strain is less than 10 %, the repeatability is satisfactory, and if the strain increases to 20 %, the repeatability decreases. Through an analysis of the resistance change of the fabric sensor during the movement of parts of the human body, such as elbows, knees, fingers, and the throat, the sensor shows satisfactory performance in monitoring human movement and physical signs.

Transforming growth factor-beta 1 (TGF-β1) suppresses T cell function, promoting tumor immune escape. Yet, whether the depression of TGF-β1 on T cell function is mediated by co-inhibitory molecules B7-H3 and B7-H4 remains largely unclear. Here, we demonstrated that TGF-β1 elevated the expression of miR-155 in colorectal cancer cells through SMAD3 and SMAD4. The upregulated miR-155 attenuated miR-143 by inhibiting its direct target, the transcription factor CEBPB. Consequently, the direct target genes of miR-143, B7-H3 and B7-H4, were augmented in the cytoplasm and membrane of tumor cells. Over-expression of B7-H3 and B7-H4 in HCT-116 cells induced T cells to secrete TGF-β1 and the immunosuppressive cytokines IL-2, IL-6, and IL-17. Restoration of miR-143 inhibited the growth of HCT-116 xenograft tumors in mice, and also repressed the expression of B7-H3 and B7-H4 in the tumors. Thus, this study reveals the mechanism by which TGF-β1 leads to T cell-mediated tumor evasion through an increase in B7-H3 and B7-H4 expression.

Myocardial ischemia/reperfusion (I/R) injury in hypercholesterolemia is associated with oxidative stress, while luteolin is known to reduce oxidative stress by activating Akt/nuclear factor erythroid-2-related factor 2 (Nrf2) signaling and alleviate cardiac I/R injury. Here, we investigated whether luteolin pretreatment diminishes myocardial I/R injury in hypercholesterolemic rats by activating Akt/Nrf2 signaling. Hypercholesterolemic rats were produced by 2% cholesterol diet for 8 weeks. Luteolin (100 mg/kg/day, i.g.) or LY294002 was administered for the last 2 weeks. The hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. Pretreatment with luteolin significantly improved left ventricular function throughout reperfusion, increased cardiac tissue viability, reduced coronary lactate dehydrogenase release and the myocardial malondialdehyde level, upregulated p-Akt and p-GSK3β expressions, inhibited nuclear translocation of Fyn, and activated Nrf2 function in hypercholesterolemic I/R rat hearts. All these improving effects of luteolin were significantly attenuated by LY294002. Ca2+-induced mitochondrial permeability transition pore (mPTP) opening and mitochondrial inner membrane potential reduction were significantly inhibited in ventricular myocytes isolated from luteolin-treated hypercholesterolemic rats, which were attenuated by LY294002. These results indicate that luteolin protects the hypercholesterolemic heart against I/R injury due to upregulation of Akt-mediated Nrf2 antioxidative function and inhibition of mPTP.

Colorectal cancer (CRC) is one of the most common malignancies in the world. Studies have demonstrated that single nucleotide polymorphisms (SNPs) in microRNA genes (miRSNPs) are involved in the occurrence of cancers. However, the relationship between the miRSNPs within the terminal-loops of microRNA precursors and the development of CRC is still largely unknown. In this study, we found that a miRSNP rs7911488 T>C in the terminal-loop of pre-miR-1307 was significantly associated with the occurrence of CRC. The C allele of rs7911488 is more prevalent in CRC patients than in healthy controls (P < 0.001), and this C allele prevalence is related to low level of miR-1307 expression. A RNA-binding protein MBNL1 binds with a 'UGCUGC' motif in the terminal-loop of the C-allelic pre-miR-1307 and blocks Dicer processing, resulting in downregulation of miR-1307 expression. Consequently, the antiapoptosis protein Bcl2, which is a direct target of miR-1307, is overexpressed in CRC. Furthermore, MBNL1 participates in processing of both C-allelic and T-allelic pre- miR-1307. In summary, our results show that rs7911488 C-allelic pre-miR-1307 binds to MBNL1 and infers with Dicer processing, leading to reduced miR-1307 and increased Bcl2 expression, thus representing an important process in the initiation of CRC.

PD-L1 is a member of the B7 family co-inhibitory molecules and plays a critical role in tumor immune escape. In this study, we found a polymorphism rs10815225 in the PD-L1 promoter region was significantly associated with the occurrence of gastric cancer. The GG homozygous frequency was higher in the cancer patients than that in the precancerous lesions, which was higher than that in the health controls. This polymorphism locates in the binding-site of Sp1 transcription factor (SP1). The expression level of PD-L1 mRNA in the GG homozygous cancer patients was apparently higher than that in the GC heterozygotes. Luciferase reporter results showed that SP1 bonded to rs10815225 G-allelic PD-L1 promoter instead of C-allelic. Upregulation and knockdown of SP1 resulted in elevation and attenuation of PD-L1 in SGC-7901 cells, respectively. The chromatin immunoprecipitation results further confirmed the binding of SP1 to the promoter of PD-L1. Additionally, rs10815225 was found to be in disequilibrium with a functional polymorphism rs4143815 in the PD-L1 3'-UTR, and the haplotypes of these two polymorphisms were also markedly related to gastric cancer risk. These results revealed a novel mechanism underlying genetic polymorphisms influencing PD-L1 expression modify gastric cancer susceptibility.

Cell wall components such as pectin and hemicelluloses have been proposed to be involved in aluminum resistance mechanisms in plants. However, whether hydroxyproline-rich glycoproteins (HRGPs), one of the most abundant proteins of the cell walls, are involved in Al resistance mechanisms remains elusive. In this study, two rice cultivars Xiushui 03 (Al resistant) and Xiushui 128 (Al sensitive) significantly differing in Al resistance were identified. In the absence of Al, no significant difference was observed in contents of glycoproteins and hydroxyproline in cell wall fractions of these two cultivars. At the early stage of Al toxicity, glycoproteins and hydroxyproline were significantly induced in these two cultivars, but levels of their accumulation in cell walls were much higher in cv. Xiushui 03 than in cv. Xiushui 128. At the late stage of Al toxicity, their accumulation in cell walls dramatically decreased in cv. Xiushui 128 and, however, still kept a high level in cv. Xiushui 03. The finding that Al-induced changes of glycoproteins and hydroxyproline were completely consistent indicates that Al-induced glycoproteins are HRGPs. Further observation utilizing transmission electron microscope showed that HRGPs were greatly accumulated in cell walls leading to thickening of cell walls in cv. Xiushui 03, however, HRGPs and cell walls greatly decreased in cv. Xiushui 128. These data suggest that Al-induced HRGP accumulation in cell walls is involved in alleviating Al toxicity in rice.

Background Rice mutant, spl5 (spotted leaf 5), has spontaneous hypersensitive-like lesions on its leaves and shows enhanced resistance to pathogens, indicating that SPL5 plays a role in programmed cell death (PCD) and disease resistance. To understand the molecular mechanism of SPL5 gene, we investigated the transcriptome profiles of the spl5 mutant leaves with few lesions (FL) and leaves with many lesions (ML) compared to the wild-type (WT) leaves respectively by microarray. Results The data from microarray revealed that 243 and 896 candidate genes (Fold change ≥ 3.0) were up- or down-regulated in the spl5-FL and spl5-ML, respectively, and a large number of these genes involved in biotic defense responses or reactive oxygen species (ROS) metabolism. Interestingly, according to our microarray and real-time PCR assays, the expressions of a transcription factor OsWRKY14 and genes responsible for the biosynthesis of serotonin, anthranilate synthase (AS), indole-3-glycerolphosphate synthase (IGPS), tryptophan synthase (TS) and tryptophan decarboxylase (TDC) were significantly up-regulated in the spl5 mutant. It has been reported previously that TS and TDC expressions are regulated by OsWRKY14 in rice, which raises the possibility that OsWRKY14 regulates serotonin production through the up-regulation of TS and TDC. Our HPLC analysis further confirmed that serotonin levels were higher in the leaves of spl5 mutant than that in WT. Conclusions Since the serotonin plays a critical role in inducing disease-resistance, the increased serotonin level may contribute, at least partly, to the disease resistance in spl5. The SPL5 gene may act as a negative regulatory factor activating the serotonin metabolic pathway, and these results might provide a new insight into the spl5-induced defense response mechanisms in plants.

Polymorphisms within the 3'-untranslated region (3'-UTR) of genes have been proved to contribute to the risk of cancers. Here, we determined 16 putatively functional polymorphisms in the 3'-UTR of 11 B7/CD28 genes in 382 colorectal cancer patients and 714 healthy controls. Statistical analysis revealed that ICOS rs4404254-C-allele carriers (p=0.0014), rs1559931-A-allele carriers (p=0.0027), and rs4675379-C-allele carriers (p=0.026) were significantly fewer in patients than those in controls. B7-H4-rs13505-GG homozygotes were more prevalent in patients (p=0.03). CD80-rs7628626-GT was apparently less in the patients with lymph node metastasis (p=0.004) or in advanced stage (p=0.037). Furthermore, we found that these polymorphisms impacted the regulatory role of miR-21-3p, miR-186-5p, miR-323b-5p, miR-1207-5p, miR-1279, miR-2117, and miR-3692-3p in the expression of the B7/CD28 molecules. Our findings suggest that rs7628626, rs13505, rs4404254, rs1559931, and rs4675379, through disrupting the regulatory role of miRNAs in the expression of B7/CD28 molecules, contribute to the occurrence and progress of colorectal cancer.

A number of single-nucleotide polymorphisms within the 3'-UTR of genes have been shown to relate to the occurrence of cancers. In this study, by using polymerase chain reaction-restriction fragment length analysis method, we determined an SNP rs1599795 in the 3'-UTR of CD80 gene in 183 gastric cancer patients and 348 healthy controls. Statistical analysis results showed that SNP rs1599795 genotypes were significantly correlated with the risk of gastric cancer. Compared with the AA homozygotes, the TA heterozygotes were significantly more prevalent in the patients (OR 1.44, 95 % CI 0.98-2.11) with a larger tumor size (P = 0.001), deeper infiltration (P = 1.5 × 10(-5)), higher possibility of lymph node metastasis (P = 0.003), and more in the late stage (TNM stage III and IV; P = 0.003); the TT homozygotes had larger tumor size (P = 0.001) and lower degree of differentiation (P = 2.2 × 10(-4)). Dual-luciferase reporter assays showed that miR-132-3p, miR-212-3p, and miR-361-5p inhibited the expression of CD80 through binding with the CD80 3'-UTR, and this inhibitory role of miR-132-3p, miR-212-3p, and miR-361-5p was impacted by rs1599795. Our findings have shown that the SNP rs1599795 in CD80 3'-UTR, through disrupting the regulatory role of miR-132-3p, miR-212-3p, and miR-361-5p in CD80 expression, contributed to the occurrence of gastric cancer.