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19 results on '"Qiao, Nan"'

2. Overexpression of chemokine receptor lymphotactin receptor 1 has prognostic value in clear cell renal cell carcinoma

Author

Xian Chang, Ya Cao, Wan‐Lei Fu, Xue‐Feng Tang, Ya‐Li Wang, Yang‐Fan Lv, and Qiao‐Nan Guo

Subjects
ccRCC, prognosis, STAT, TCGA, XCR1, Genetics, QH426-470
Abstract

Abstract Background Clear cell renal cell carcinoma (ccRCC) is an aggressive subtype of renal cell carcinoma. X‐C motif chemokine receptor 1 (XCR1) exerts important roles in tumor progression; however, its role in ccRCC is unclear. Methods We utilized publicly available data from The Cancer Genome Atlas (TCGA) to assess the role of XCR1 in ccRCC and validated the results in 36 samples from patients with ccRCC who underwent curative resection in Xinqiao Hospital Chongqing. XCR1 overexpression was identified in ccRCC, which was confirmed by qRT‐PCR assay and immunohistochemical staining of ccRCC samples. Results For the TCGA and clinical data, Kaplan–Meier survival analysis revealed that higher XCR1 expression in ccRCC was related to longer overall survival. Cox regression analysis suggested that XCR1 is an independent risk factor for ccRCC. GSEA analysis suggested that XCR1 is associated with the JAK/STAT signaling pathway. XCR1 knockdown by small interfering RNA (siRNA) significantly increased ccRCC cell proliferation and migration, and decreased cell apoptosis. Conclusion We found higher XCR1 expression in ccRCC compared with that in normal tissues is related to longer overall survival in patients with ccRCC. XCR1 knockdown significantly increased RCC cells proliferation and migration, and decreased apoptosis. XCR1 might be used as a prognostic biomarker in ccRCC in the future.

Published
2021
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9. Identification of SRY‐box 30 as an age‐related essential gatekeeper for male germ‐cell meiosis and differentiation

Author

Han, Fei, primary, Yin, Li, additional, Jiang, Xiao, additional, Zhang, Xi, additional, Zhang, Ning, additional, Yang, Jun‐tang, additional, Ouyang, Wei‐ming, additional, Hao, Xiang‐lin, additional, Liu, Wen‐bin, additional, Huang, Yong‐sheng, additional, Chen, Hong‐qiang, additional, Gao, Fei, additional, Li, Zhong‐tai, additional, Guo, Qiao‐nan, additional, Cao, Jia, additional, and Liu, Jin‐yi, additional

Published
2021
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12. The risk of new‐onset cancer associated with <scp>HFE</scp> C282Y and H63D mutations: evidence from 87,028 participants

Author

Rui-Xi Hua, Gang Meng, Xi Zhang, Xian Chang, Guang-Ning Yan, Xiao‐Yu Liao, Yang-Fan Lv, and Qiao-Nan Guo

Subjects
Oncology, medicine.medical_specialty, Colorectal cancer, Bioinformatics, Polymorphism, Single Nucleotide, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Breast cancer, Risk Factors, Neoplasms, Internal medicine, Genetic model, Odds Ratio, hereditary haemochromatosis, cancer, Humans, Medicine, Missense mutation, Genetic Predisposition to Disease, H63D, Allele, Hemochromatosis Protein, business.industry, Case-control study, Cancer, Original Articles, Cell Biology, Odds ratio, medicine.disease, C282Y, meta‐analysis, Case-Control Studies, 030220 oncology & carcinogenesis, Mutation, Molecular Medicine, Original Article, 030211 gastroenterology & hepatology, HFE, business, Publication Bias
Abstract

To investigate the association between mutation of HFE (the principal pathogenic gene in hereditary haemochromatosis) and risk of cancer, we conducted a meta‐analysis of all available case–control or cohort studies relating to two missense mutations, C282Y and H63D mutations. Eligible studies were identified by searching databases including PubMed, Embase and the ISI Web of Knowledge. Overall and subgroup analyses were performed and odds ratios (ORs) combined with 95% confidence intervals (CIs) were applied to evaluate the association between C282Y mutation, H63D mutation and cancer risk. Sensitivity and cumulative analyses were used to evaluate the stability of the results. A total of 36 eligible studies were included, comprising 13,680 cases and 73,348 controls. C282Y was significantly associated with elevated cancer risk in a recessive genetic model (OR: 1.991, 95% CI: 1.448–2.737). On subgroup analysis stratified by cancer type, statistically significantly increased cancer risks were found for breast cancer, colorectal cancer and hepatocellular carcinoma in a recessive model. When stratified by territory, a significantly increased risk of cancer was found in Oceanic populations in a recessive model and in Asian populations in an allele model and dominant model. H63D mutation did not significantly increase overall cancer risk in any genetic model. However, when, stratified by territory, an increased cancer risk was found in the Asian population in an allele and dominant. C282Y but not H63D mutation was related to elevated cancer risk. Further large‐scale studies considering gene–environment interactions and functional research should be conducted to further investigate this association.

Published
2016

14. Endothelial cells promote stem‐like phenotype of glioma cells through activating the Hedgehog pathway

Author

You-Hong Cui, De-Yu Guo, Guang-Ning Yan, Lang Yang, Xiu-Wu Bian, Xia Zhang, Xiao-Hong Yao, Yu Shi, Yang-Fan Lv, Qiao-Nan Guo, Peng Zhang, and Li-Li Shen

Subjects
Male, glioma stem cell, Pathology and Forensic Medicine, Mice, hedgehog pathway, SOX2, Antigens, CD, Cancer stem cell, GLI1, Cell Line, Tumor, Glioma, Tumor Microenvironment, medicine, Animals, Humans, Hedgehog Proteins, AC133 Antigen, Stem Cell Niche, neoplasms, Glycoproteins, Tumor microenvironment, biology, Brain Neoplasms, Endothelial Cells, Middle Aged, Allografts, medicine.disease, Original Papers, Hedgehog signaling pathway, nervous system diseases, Gene Expression Regulation, Neoplastic, Endothelial stem cell, niche, Phenotype, endothelial cell, Neoplastic Stem Cells, Cancer research, biology.protein, Female, Stem cell, Glioblastoma, Peptides, Signal Transduction
Abstract

Microenvironmental regulation of cancer stem cells (CSCs) strongly influences the onset and spread of cancer. The way in which glioma cells interact with their microenvironment and acquire the phenotypes of CSCs remains elusive. We investigated how communication between vascular endothelial cells and glioma cells promoted the properties of glioma stem cells (GSCs). We observed that CD133+ GSCs were located closely to Shh+ endothelial cells in specimens of human glioblastoma multiforme (GBM). In both in vitro and in vivo studies, we found that endothelial cells promoted the appearance of CSC-like glioma cells, as demonstrated by increases in tumourigenicity and expression of stemness genes such as Sox2, Olig2, Bmi1 and CD133 in glioma cells that were co-cultured with endothelial cells. Knockdown of Smo in glioma cells led to a significant reduction of their CSC-like phenotype formation in vitro and in vivo. Endothelial cells with Shh knockdown failed to promote Hedgehog (HH) pathway activation and CSC-like phenotype formation in co-cultured glioma cells. By examination of glioma tissue specimens from 65 patients, we found that the survival of glioma patients was closely correlated with the expression of both Shh by endothelial cells and Gli1 by perivascular glioma cells. Taken together, our study demonstrates that endothelial cells in the tumour microenvironment provide Shh to activate the HH signalling pathway in glioma cells, thereby promoting GSC properties and glioma propagation. © 2014 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Published
2014

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