Wang R.,Xian Jiaotong University |
Zhang J.,Xian Jiaotong University |
Qin Q.,Xian Jiaotong University |
Liu L.,Xian Jiaotong University |
And 5 more authors.
Journal of Xi'an Jiaotong University (Medical Sciences)
Objective: To detect the expression of Foxp3 in both peripheral blood mononuclears (PBMCs) and thyroid tissues of patients with autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT) so as to evaluate the relationship between regulatory T cells (Treg) and pathogenesis of AITD. Methods: Foxp3 mRNA level was measured by real-time PCR from PBMCs and thyroid tissues of AITD patients and normal controls; Foxp3 protein expression was detected both by a standard immunohistochemical procedure from thyroid tissues and by western blot from PBMCs. Results: Foxp3 mRNA level in PBMCs from AITD patients significantly decreased compared with that in normal controls (P<0.05); Foxp3 protein expression was lower only in HT patients from PBMCs, but not in GD patients (P>0.05). Foxp3 mRNA and protein levels were higher in thyroid tissues of HT patients than in normal tissues (P<0.05), but did not differ significantly in thyroid tissues from GD patients (P>0.05). Conclusion: The lower expression of Foxp3 in AITD patients suggests that the decreased number of CD4 +CD25 +Foxp3 +Tregs or dysfunction of these cells may be involved in the development of AITD, especially in HT. Source
Jiang Z.,The First Hospital of Yulin City |
Hao Y.,The First Hospital of Yulin City |
Ding X.,The First Hospital of Yulin City |
Zhang Z.,The First Hospital of Yulin City |
And 3 more authors.
A novel paradigm in tumor biology suggests that non-small cell lung cancer (NSCLC) growth is driven by lung cancer stem cell-like cells (LCSCs), but molecular mechanisms regulating tumorigenic and self-renewal potential of LCSCs are still unclear. Here, we aim to investigate biological function of SLC34A2 in regulating tumorigenicity of LCSCs and its underlying mechanisms. Our findings testified that CD166+ cells which were derived from fresh primary NSCLC samples displayed stem cell-like features. Fluorescence-activated cell sorting (FACS) analysis showed the presence of a variable fraction of CD166 cells in 15 out of 15 NSCLC samples. Significantly, CD166+ LCSCs from primary NSCLC tumors expressed high level of SLC34A2 which was required for CD166+ LCSCs tumorigenic and self-renewal potential. In NSCLC patient cohort, increased SLC34A2 expression correlated with histology, which suggests a potential role of SLC34A2 in CD166+ LCSCs. Furthermore, Wnt/β-catenin pathway and Bmi1 were found necessary for tumorigenicity and self-renewal capacity of CD166+ LCSCs by a series in vitro and in vivo experiments. Then, our study indicated that SLC34A2 regulated Bmi1 to promote tumorigenic and self-renewal potential of CD166+ LCSCs through Wnt/β-catenin pathway. In this study, the characterization of molecular basis of SLC34A2 in CD166+ LCSCs not only allows for better understanding of the mechanisms regulating tumorigenicity of this specific population of NSCLC cells but also provides insight into the gradual improvement of more effective cancer therapies against this disease. © 2016 International Society of Oncology and BioMarkers (ISOBM) Source