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Li K.,Guangxi Medical University | Du Y.,Guangxi Medical University | Jiang B.-L.,First Peoples Hospital of Nanning | He J.-F.,Guangxi Medical University
Medical Science Monitor | Year: 2014

Graves' ophthalmopathy is an inflammatory autoimmune disease of the orbit, characterized by inflammation and proliferation of the orbital tissue caused by CD4+T cells and orbital fibroblasts. Despite recent substantial findings regarding its cellular and molecular foundations, the pathogenesis of Graves' ophthalmopathy remains unclear. Accumulating data suggest that microRNAs play important roles in the pathophysiology of autoimmunity and proliferation. Specifically, microRNA-155 (miR-155) can promote autoimmune inflammation by enhancing inflammatory T cell development. In contrast to miR-155, microRNA-146a (miR-146a) can inhibit the immune response by suppressing T cell activation. Furthermore, miR-155 and miR-146a are involved in cell proliferation, differentiation, and many other life processes. Thus, miR-155 and miR-146a, with opposite impacts on inflammatory responses carried out by T lymphocytes, appear to have multiple targets in the pathogenesis of Graves' ophthalmopathy. Our previous work showed that the expression of miR-146a was significantly decreased in peripheral blood mononuclear cells from Graves' ophthalmopathy patients compared with normal subjects. Accordingly, we proposed that the expression of miR-155 increased and the expression of miR-146a decreased in the target cells (CD4+T cells and orbital fibroblasts), thus promoting ocular inflammation and proliferation in Graves' ophthalmopathy. The proposed hypothesis warrants further investigation of the function of the differentially expressed microRNAs, which may shed new light on the pathogenesis of Graves' ophthalmopathy and lead to new strategies for its management. © Med Sci Monit, 2014. Source

Duan M.-C.,Eighth Peoples Hospital of Nanning | Zhong X.-N.,Guangxi Medical University | Liu G.-N.,Guangxi Medical University | Wei J.-R.,First Peoples Hospital of Nanning
Journal of Immunology Research | Year: 2014

Pathogenic mechanisms underlying the development of lung cancer are very complex and not yet entirely clarified. T lymphocytes and their immune-regulatory cytokines play a pivotal role in controlling tumor growth and metastasis. Following activation by unique cytokines, CD4+ T helper cells differentiate into Th1, Th2, Th17, and regulatory T cells (Tregs). Traditionally, research in lung cancer immunity has focused almost exclusively on Th1/Th2 cell balance. Recently, Th17 cells and Tregs represent an intriguing issue to be addressed in lung cancer pathogenesis. Tregs play an important role in the preservation of self-tolerance and modulation of overall immune responses against tumor cells. Th17 cells directly or via other proinflammatory cytokines modulate antitumor immune responses. Notably, there is a close relation between Tregs and Th17 cells. However, the possible interaction between these subsets in lung cancer remains to be elucidated. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent a useful tool for lung cancer treatment in the future. The purpose of this review is to discuss recent findings of the role of these novel populations in lung cancer immunity and to highlight the pleiotropic effects of these subsets on the development and regulation of lung cancer. © 2014 Min-Chao Duan et al. Source

Li Z.,Kunming Medical University | Yang Y.,First Peoples Hospital of Nanning | Gao Y.,Kunming Medical University | Wu X.,Kunming Medical University | And 6 more authors.
American Journal of Cancer Research | Year: 2016

Accumulating evidence has revealed that the expression of the lipid raft protein flotillin-1 is elevated in various human cancers, but the role flotillin-1 plays in the carcinogenesis of cervical cancer remains unclear. The expression profile of flotillin-1 was assayed using real-time PCR, western blotting, and immunohistochemical (IHC) staining in cervical cancer cell lines and cancer tissues with paired adjacent noncancerous cervical tissues. The expression of flotillin-1 protein was detected by IHC staining in a large cohort of 308 paraffin-embedded cervical cancer tissues. Ectopic expression and the short hairpin RNA interference approach were employed to determine the role of flotillin-1 in cervical cancer cell metastasis and the possible mechanism involved. Flotillin-1 expression protein and mRNA were significantly upregulated in cervical cancer cell lines and cancer tissues; elevated expression of flotillin-1 protein in early-stage cervical cancer was significantly associated with pelvic lymph node metastasis (P < 0.001), and was an independent predictive factor of poor overall survival. Moreover, flotillin-1 up- and downregulation remarkably affected cervical cancer cell motility and invasion, respectively, through epithelial-mesenchymal transition (EMT) regulated by the Wnt/β-catenin and nuclear factor-κB (NF-κB) pathways. Our results suggest that flotillin-1 facilitates cervical cancer cell metastasis through Wnt/β-catenin and NF-κB pathway-regulated EMT and that the flotillin-1 expression profile serves not only as novel predictor of pelvic lymph node metastasis, but also as neoteric risk factor for patients with early-stage cervical cancer. Source

Qin Y.,Guangxi Medical University | Li L.,Guangxi Medical University | Chen J.,Guangxi Medical University | Tang X.,First Peoples Hospital of Nanning | And 3 more authors.
Oncology Research | Year: 2012

Fentanyl is used as an analgesic to treat pain in a variety of patients with cancer. Moreover, fentanyl may affect tumor growth in many cell lines. To gain better insight into the interaction between fentanyl and tumor, we investigated the effects of fentanyl on the growth of gastric carcinoma cells and the expression of some apoptosis-related genes including NF-κB and PTEN. A human gastric cancer cell line MGC-803 was used. The viability and proliferation of gastric cancer MGC-803 cells were detected by MTT assay and colony formation assay. The cell cycle progression and apoptosis were assessed by flow cytometry and the ultrastructure of cells was examined with transmission electron microscope. The migration of cells was investigated by wound healing assay. The expression of NF-κB and PTEN was evaluated by semiquantitative RT-PCR and Western blot. Our data showed that fentanyl could inhibit cell growth and proliferation and made cell cycle arrest at G2/M phase. Compared with control cells, MGC-803 cells that were incubated with fentanyl also had a higher apoptotic rate. Fentanyl could lead to morphological changes of gastric cancer cells and reduce the motility of MGC-803 cells. Moreover, fentanyl could downregulate NF-κB and upregulate PTEN, which might be the mechanism of fentanyl inhibiting gastric cancer progression in vitro. Copyright © 2012 Cognizant Comm. Corp. Source

Su S.Y.,Guangxi Medical University | Zhou X.,Guangxi Medical University | Pang X.M.,First Peoples Hospital of Nanning | Chen C.Y.,Guangxi Medical University | And 2 more authors.
Genetics and Molecular Research | Year: 2016

Neurofibromatosis type 1, also known as NF1 or von Recklinghausen’s disease, is a common neurocutaneous syndrome that presents with multiple café-au-lait patches, skinfold freckling, dermatofibromas, neurofibromas, and Lisch nodules. The mutations of the gene NF1, encoding the protein neurofibromin, have been identified as the cause of this disease. Here, we report a clinical and molecular study of a Chinese patient with multiple café-au-lait skin freckles, dermatofibroma, central and peripheral nervous system tumors, and bone abnormalities attributed to NF1. The patient showed >6 café-au-lait spots on the body and multiple dermatofibromas. A brain glioma and multiple nerve sheath tumors inside and outside the vertebral canal were identified by magnetic resonance imaging, which also showed multiple intercostal nerve schwannomas and hydrocephalies above the cerebellar tentorium. Talipes equinus was also apparent. A mutation analysis of the NF1 gene revealed a novel frameshift mutation in exon 43, consisting of a heterozygous deletion of four nucleotides (GAGA) between positions 6520 and 6523. No NF1 mutations were detected in the patient’s parents or younger brother. These results extend the list of known mutations in this gene. The absence of the NF1 mutation in the healthy family members suggests that it is responsible for the NF1 phenotype. To our knowledge, this frameshift mutation represents a novel NF1 case, and may be associated with nervous system tumors and bone abnormalities. © FUNPEC-RP. Source

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