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  • 1
    Online Resource
    Online Resource
    Behçet’s disease: An immunogenetic perspective
    Wiley ; 2019
    In:  Journal of Cellular Physiology Vol. 234, No. 6 ( 2019-06), p. 8055-8074
    Details
    In: Journal of Cellular Physiology, Wiley, Vol. 234, No. 6 ( 2019-06), p. 8055-8074
    Abstract: Behçet’s disease (BD) is a chronic and rare multisystemic disorder defined by autoimmunity and inflammatory characteristics, manifested by ocular lesions, recurrent genital and oral ulcers, skin symptoms and arthritis as well as neurological, intestinal, and vascular involvement. Despite the unknown cause of BD, there is some strong documentation for immunological, genetic, environmental, and infectious factors playing a role in the pathogenesis of BD. While the nature of the genetic variants remains unidentified, many genetic risk factors are considered to contribute to BD susceptibility. Along with human leukocyte antigen gene encoding B*51 (HLA‐B*51) and areas including the major histocompatibility complex class I, genome‐wide association studies have recognized numerous other BD susceptibility genes including those encoding interleukin (IL)‐10, IL‐12 receptor β 2 (IL‐12RB2), IL‐23 receptor (IL‐23R), C‐C chemokine receptor 1 gene, signal transducer and activator of transcription 4 (STAT4), endoplasmic reticulum aminopeptidase (ERAP1), and genes encoding killer cell lectin‐like receptor family members (KLRC4‐KLRK1). It is believed that BD could be considered as a disorder lying in between autoimmune and autoinflammatory syndromes. The positive responses to classical immunosuppressive agents like azathioprine and cyclosporine and involvement of autoantigens in the initiation of the disorder are the main BD features that reflect the autoimmune nature of the disorder. In this review, we address recent findings on the role of common cytokines, antibodies and immunogenetic factors in BD.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    URL: Article
    DOI: 10.1002/jcp.v234.6
    DOI: 10.1002/jcp.27576
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Probiotics as a Therapeutic Approach in Colorectal Cancer
    Bentham Science Publishers Ltd. ; 2023
    In:  Current Cancer Drug Targets Vol. 23, No. 10 ( 2023-11), p. 764-777
    Details
    In: Current Cancer Drug Targets, Bentham Science Publishers Ltd., Vol. 23, No. 10 ( 2023-11), p. 764-777
    Abstract: Colorectal cancer (CRC) is a growing concern worldwide. In recent decades, the incidence of CRC has increased, and this has been attributed to changes in lifestyle. The lack of physical activity, smoking habits, and a diet high in red meat and fat and low in fiber are important aspects of these deleterious changes in lifestyle. The increase in the incidence of CRC has impelled researchers to investigate methods for preventing and treating CRC with greater efficacy and fewer complications. Probiotics are an attractive and potentially promising therapeutic approach. They have been evaluated by a large number of preclinical and clinical studies in recent years, and it has been found that they can play a role in the prevention, treatment, and management of complications of CRC. This review provides a concise summary of the mechanisms of action of probiotics. Furthermore, it focuses on the results of clinical and preclinical studies that evaluated probiotics' effects on CRC management. It also discusses the effects of different strains of probiotics and their combination in CRC treatment.
    Type of Medium: Online Resource
    ISSN: 1568-0096
    URL: Article
    DOI: 10.2174/1568009623666230413081513
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2023
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    The association between HPV gene expression, inflammatory agents and cellular genes involved in EMT in lung cancer tissue
    Springer Science and Business Media LLC ; 2020
    In:  BMC Cancer Vol. 20, No. 1 ( 2020-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 20, No. 1 ( 2020-12)
    Abstract: Lung cancer is a leading cause of cancer morbidity and mortality worldwide. Several studies have suggested that Human papillomavirus (HPV) infection is an important risk factor in the development of lung cancer. In this study, we aim to address the role of HPV in the development of lung cancer mechanistically by examining the induction of inflammation and epithelial-mesenchymal transition (EMT) by this virus. Methods In this case-control study, tissue samples were collected from 102 cases with lung cancer and 48 controls. We examined the presence of HPV DNA and also the viral genotype in positive samples. We also examined the expression of viral genes (E2, E6 and E7), anti-carcinogenic genes (p53, retinoblastoma (RB)), and inflammatory cytokines in HPV positive cases. Results HPV DNA was detected in 52.9% (54/102) of the case samples and in 25% (12/48) of controls. A significant association was observed between a HPV positive status and lung cancer ( OR = 3.37, 95% C.I = 1.58–7.22, P = 0.001 ). The most prevalent virus genotype in the patients was type 16 (38.8%). The expression of p53 and RB were decreased while and inflammatory cytokines were increased in HPV-positive lung cancer and HPV-positive control tissues compared to HPV-negative lung cancer and HPV-negative control tissues. Also, the expression level of E-cad and PTPN-13 genes were decreased in HPV- positive samples while the expression level of SLUG, TWIST and N-cad was increased in HPV-positive samples compared to negative samples. Conclusion Our study suggests that HPV infection drives the induction of inflammation and EMT which may promote in the development of lung cancer.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/s12885-020-07428-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2041352-X
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  • 4
    Online Resource
    Online Resource
    Expression Analysis of Five Different Long Non-Coding Ribonucleic Acids in Nonsmall-Cell Lung Carcinoma Tumor and Tumor-Derived Exosomes
    MDPI AG ; 2022
    In:  Diagnostics Vol. 12, No. 12 ( 2022-12-17), p. 3209-
    Details
    In: Diagnostics, MDPI AG, Vol. 12, No. 12 ( 2022-12-17), p. 3209-
    Abstract: Long non-coding ribonucleic acids (LncRNAs) are recently known for their role in regulating gene expression and the development of cancer. Controversial results indicate a correlation between the tissue expression of LncRNA and LncRNA content of extracellular vesicles. The present study aimed to evaluate the expression of different LncRNAs in non-small cell lung cancer (NSCLC) patients in tumor tissue, adjacent non-cancerous tissue (ANCT), and exosome-mediated lncRNA. Tumor and ANCT, as well as serum samples of 168 patient with NSCLC, were collected. The GHSROS, HNF1A-AS1, HOTAIR, HMlincRNA717, and LINCRNA-p21 relative expressions in tumor tissue, ANCT, and serum exosomes were evaluated in NSCLC patients. Among 168 NSCLC samples, the expressions of GHSROS (REx = 3.64, p = 0.028), HNF1A-AS1 (REx = 2.97, p = 0.041), and HOTAIR (REx = 2.9, p = 0.0389) were upregulated, and the expressions of HMlincRNA717 (REx = −4.56, p = 0.0012) and LINCRNA-p21 (REx = −5.14, p = 0.00334) were downregulated in tumor tissue in contrast to ANCT. Moreover, similar statistical differences were seen in the exosome-derived RNA of tumor tissues in contrast to ANCT samples. A panel of the five lncRNAs demonstrated that the area under the curve (AUC) for exosome and tumor was 0.937 (standard error: 0.012, p value 〈 0.0001). LncRNAs GHSROS, HNF1A-AS1, and HOTAIR showed high expression in tumor tissue and exosome content in NSCLC, and a panel that consisted of all five lncRNAs improved diagnosis of NSCLC.
    Type of Medium: Online Resource
    ISSN: 2075-4418
    URL: Article
    DOI: 10.3390/diagnostics12123209
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2662336-5
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  • 5
    Online Resource
    Online Resource
    MicroRNA and exosome: Key players in rheumatoid arthritis
    Wiley ; 2019
    In:  Journal of Cellular Biochemistry Vol. 120, No. 7 ( 2019-07), p. 10930-10944
    Details
    In: Journal of Cellular Biochemistry, Wiley, Vol. 120, No. 7 ( 2019-07), p. 10930-10944
    Abstract: Rheumatoid arthritis (RA) is known as one of important autoimmune disorders which can lead to joint pain and damage throughout body. Given that internal (ie, genetic and epigenetic alterations) and external factors (ie, lifestyle changes, age, hormones, smoking, stress, and obesity) involved in RA pathogenesis. Increasing evidence indicated that cellular and molecular alterations play critical roles in the initiation and progression of RA. Among various targets and molecular signaling pathways, microRNAs (miRNAs) and their regulatory networks have key roles in the RA pathogenesis. It has been showed that deregulation of many miRNAs involved in different stages of RA. Hence, identification of miRNAs and their signaling pathways in RA, could contribute to new knowledge which help to better treatment of patients with RA. Besides miRNAs, exosomes have been emerged as key messengers in RA pathogenesis. Exsosomes are nanocarriers which could be released from various cells and lead to changing of behaviors recipient cells via targeting their cargos (eg, proteins, messenger RNAs, miRNAs, long noncoding RNAs, DNAs). Here, we summarized several miRNAs involved in RA pathogenesis. Moreover, we highlighted the roles of exosomes in RA pathogenesis.
    Type of Medium: Online Resource
    ISSN: 0730-2312 , 1097-4644
    URL: Issue
    URL: Article
    DOI: 10.1002/jcb.v120.7
    DOI: 10.1002/jcb.28499
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1479976-5
    SSG: 12
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