24 results on '"Guan, Xin-Yuan"'
Search Results
2. Long non-coding RNA NEAT1 mediated RPRD1B stability facilitates fatty acid metabolism and lymph node metastasis via c-Jun/c-Fos/SREBP1 axis in gastric cancer
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Jia, Yongxu, Yan, Qian, Zheng, Yinli, Li, Lei, Zhang, Baifeng, Chang, Zhiwei, Wang, Zehua, Tang, Hong, Qin, Yanru, and Guan, Xin-Yuan
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- 2022
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3. PITX2C increases the stemness features of hepatocellular carcinoma cells by up-regulating key developmental factors in liver progenitor
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Jiang, Lingxi, Wang, Xia, Ma, Fangfang, Wang, Xuelong, Shi, Minmin, Yan, Qian, Liu, Ming, Chen, Juan, Shi, Chaoran, and Guan, Xin-yuan
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- 2022
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4. Targeting TROY-mediated P85a/AKT/TBX3 signaling attenuates tumor stemness and elevates treatment response in hepatocellular carcinoma
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Liu, Beilei, Fang, Xiaona, Kwong, Dora Lai-Wan, Zhang, Yu, Verhoeft, Krista, Gong, Lanqi, Zhang, Baifeng, Chen, Jie, Yu, Qianqian, Luo, Jie, Tang, Ying, Huang, Tuxiong, Ling, Fei, Fu, Li, Yan, Qian, and Guan, Xin-Yuan
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- 2022
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5. PARP inhibitor Olaparib overcomes Sorafenib resistance through reshaping the pluripotent transcriptome in hepatocellular carcinoma
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Yang, Xiao-Dong, Kong, Fan-En, Qi, Ling, Lin, Jia-Xin, Yan, Qian, Loong, Jane Ho Chun, Xi, Shao-Yan, Zhao, Yue, Zhang, Yan, Yuan, Yun-Fei, Ma, Ning-Fang, Ma, Stephanie, Guan, Xin-Yuan, and Liu, Ming
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- 2021
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6. Correction to: CircLONP2 enhances colorectal carcinoma invasion and metastasis through modulating the maturation and exosomal dissemination of microRNA-17
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Han, Kai, Wang, Feng-Wei, Cao, Chen-Hui, Ling, Han, Chen, Jie-Wei, Chen, Ri-Xin, Feng, Zi-Hao, Luo, Jie, Jin, Xiao-Han, Duan, Jin-Ling, Li, Shu-Man, Ma, Ning-Fang, Yun, Jing-Ping, Guan, Xin-Yuan, Pan, Zhi-Zhong, Lan, Ping, Xu, Rui-Hua, and Xie, Dan
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- 2021
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7. Molecular subclassification of gastrointestinal cancers based on cancer stem cell traits
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Li, Mei-Mei, Yuan, Jun, Guan, Xin-Yuan, Ma, Ning-Fang, and Liu, Ming
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- 2021
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8. CircLONP2 enhances colorectal carcinoma invasion and metastasis through modulating the maturation and exosomal dissemination of microRNA-17
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Han, Kai, Wang, Feng-Wei, Cao, Chen-Hui, Ling, Han, Chen, Jie-Wei, Chen, Ri-Xin, Feng, Zi-Hao, Luo, Jie, Jin, Xiao-Han, Duan, Jin-Ling, Li, Shu-Man, Ma, Ning-Fang, Yun, Jing-Ping, Guan, Xin-Yuan, Pan, Zhi-Zhong, Lan, Ping, Xu, Rui-Hua, and Xie, Dan
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- 2020
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9. SOX9 is a dose-dependent metastatic fate determinant in melanoma
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Yang, Xintao, Liang, Rui, Liu, Chunxi, Liu, Jessica Aijia, Cheung, May Pui Lai, Liu, Xuelai, Man, On Ying, Guan, Xin-Yuan, Lung, Hong Lok, and Cheung, Martin
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- 2019
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10. Development of an oncogenic dedifferentiation SOX signature with prognostic significance in hepatocellular carcinoma
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Li, Mei-Mei, Tang, Yun-Qiang, Gong, Yuan-Feng, Cheng, Wei, Li, Hao-Long, Kong, Fan-En, Zhu, Wen-Jie, Liu, Shan-Shan, Huang, Li, Guan, Xin-Yuan, Ma, Ning-Fang, and Liu, Ming
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- 2019
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11. H3K27me3 Protein Is a Promising Predictive Biomarker of Patients’ Survival and Chemoradioresistance in Human Nasopharyngeal Carcinoma
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Cai, Mu-Yan, Tong, Zhu-Ting, Zhu, Wei, Wen, Zhu-Zhi, Rao, Hui-Lan, Kong, Ling-Ling, Guan, Xin-Yuan, Kung, Hsiang-Fu, Zeng, Yi-Xin, and Xie, Dan
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- 2011
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12. High Expression of H3K27me3 in Human Hepatocellular Carcinomas Correlates Closely with Vascular Invasion and Predicts Worse Prognosis in Patients
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Cai, Mu-Yan, Hou, Jing-Hui, Rao, Hui-Lan, Luo, Rong-Zhen, Li, Mei, Pei, Xiao-Qing, Lin, Marie C., Guan, Xin-Yuan, Kung, Hsiang-Fu, Zeng, Yi-Xin, and Xie, Dan
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- 2011
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13. CD133+ liver cancer stem cells resist interferon-gamma-induced autophagy.
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Jian Li, Jin-Na Chen, Ting-Ting Zeng, Fan He, Shu-Peng Chen, Stephanie Ma, Jiong Bi, Xiao-Feng Zhu, Xin-Yuan Guan, Li, Jian, Chen, Jin-Na, Zeng, Ting-Ting, He, Fan, Chen, Shu-Peng, Ma, Stephanie, Bi, Jiong, Zhu, Xiao-Feng, and Guan, Xin-Yuan
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CD antigens ,LIVER cancer ,CANCER stem cells ,INTERFERON gamma ,AUTOPHAGY ,ANIMAL experimentation ,ANTIGENS ,CELL lines ,CELL physiology ,GENES ,GLYCOPROTEINS ,HEPATOCELLULAR carcinoma ,INTERFERONS ,LIVER tumors ,MICE ,PEPTIDES ,STEM cells - Abstract
Background: Hepatocellular carcinoma (HCC) is one of the most fatal malignancies worldwide, and CD133 is a popular cancer stem cell (CSC) marker for HCC. CD133(+) CSCs have been reported to resist conventional chemo- and radiotherapy, but little is known about their response to immune surveillance. Interferon-gamma (IFN-γ) is one of key cytokines that the immune system produce to eradicate cancer cells, so we investigated the function of IFN-γ on CD133+ HCC CSCs in this study.Methods: The response of CD133(+) cells to IFN-γ was performed with functional assays (cell proliferation assay and tumor formation in nude mice), flow cytometry, immunofluorescence staining and RNA interference.Results: We found that IFN-γ inhibited the proliferation of cell lines with low percentage of CD133(+) cells (wild-type human cells, BEL7402, QGY7701) but it did not affect the proliferation of cell lines with high percentage of CD133(+) cells (wild-type human cells, Huh7, PLC8024) in vivo and in vitro (nude mice). Flow cytometry analysis demonstrated that the percentage of CD133+ cells increased after IFN-γ treatment of low CD133(+) cell lines. Furthermore, IFN-γ induced the autophagy of low CD133(+) cell lines to decrease proliferation.Conclusion: CD133(+) HCC CSCs resisted IFN-γ-induced autophagy, which might also be a mechanism through which CSCs resist immune eradication. [ABSTRACT FROM AUTHOR]- Published
- 2016
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14. CHD1L Protein is overexpressed in human ovarian carcinomas and is a novel predictive biomarker for patients survival.
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He, Wei-Peng, Zhou, Juan, Cai, Mu-Yan, Xiao, Xiang-Shen, Liao, Yi-Ji, Kung, Hsiang-Fu, Guan, Xin-Yuan, Xie, Dan, and Yang, Guo-Fen
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DNA-binding proteins ,LIVER cancer ,OVARIAN cancer ,IMMUNOHISTOCHEMISTRY ,PROTEINS ,BIOMARKERS - Abstract
Background: Our recent studies suggested that the chromodomain helicase DNA binding protein 1-like (CHD1L) gene plays an oncogenic role in human hepatocellular carcinoma. However, the status of CHD1L protein expression in ovarian cancer and its clinical/prognostic significance are obscure. Methods: In this study, immunohistochemistry (IHC) for CHD1L was performed on a tissue microarray (TMA) containing 102 primary ovarian carcinomas and 44 metastatic lesions (omental metastasis). Receiver-operator curve (ROC) analysis was used to evaluate patients’ survival status. Results: There is an augmented tendency of CHD1L expression in ovarian carcinoma metastasis than in primary lesions (P<0.05). A significant association was found between positive expression of CHD1L and tumors histological type (P <0.05). By univariate survival analysis of the ovarian carcinoma cohorts, positive expression of CHD1L was significantly correlated with shortened patient survival (mean 66.7 months versus 97.4 months, P<0.05). Moreover, CHD1L expression was evaluated to be a significant and independent prognostic factor in multivariate analysis (P<0.05). Conclusions: These findings provide evidence that positive expression of CHD1L protein is significantly correlated with the metastasis proceeding of ovarian carcinoma, and CHD1L protein expression, as examined by IHC, may act as a novel prognostic biomarker for patients with ovarian carcinoma. [ABSTRACT FROM AUTHOR]
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- 2012
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15. Prognostic impact of H3K27me3 expression on locoregional progression after chemoradiotherapy in esophageal squamous cell carcinoma.
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He LR, Liu MZ, Li BK, Rao HL, Liao YJ, Guan XY, Zeng YX, Xie D, He, Li-Ru, Liu, Meng-Zhong, Li, Bin-Kui, Rao, Hui-Lan, Liao, Yi-Ji, Guan, Xin-Yuan, Zeng, Yi-Xin, and Xie, Dan
- Abstract
Background: Trimethylation of lysine 27 on histone H3 (H3K27me3) by enhancer of zeste homolog 2 (EZH2) is an epigenetic mark that mediates gene silencing. EZH2 is overexpressed and correlates with poor prognosis in many cancers. However, the clinical implication of H3K27me3 in human malignancies has not been well established. We wished to ascertain whether a correlation exists between the expression of H3K27me3 and clinical outcome in a group of patients with esophageal squamous cell carcinoma (ESCC) treated with definitive chemoradiotherapy (CRT).Methods: The method of immunohistochemistry (IHC) was utilized to examine the protein expression of H3K27me3 in 98 pretreatment biopsy specimens of ESCC and in 30 samples of normal esophageal mucosa. The clinical/prognostic significance of H3K27me3 expression was statistically analyzed.Results: The expression frequency and expression levels of H3K27me3 were significantly higher in ESCCs than in normal tissues. There was a positive correlation between H3K27me3 expression and WHO grade (P = 0.016), tumor size (P = 0.019), T status (P = 0.024), locoregional progression (P = 0.009) and EZH2 expression (P = 0.036). High H3K27me3 expression was associated with poor locoregional progression-free survival (LPFS) (P = 0.010) in ESCC. Further analysis demonstrated that H3K27me3 could stratify patient outcome in T2-3 (P = 0.048), N0 (P = 0.005) and M0 (P = 0.018) stages as well as in CRT effective group (P = 0.022).Conclusions: Our data suggests that H3K27me3 expression examined by IHC might be useful for stratifying LPFS for different subsets of ESCC patients treated with definitive CRT. [ABSTRACT FROM AUTHOR]- Published
- 2009
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16. Expression of EIF5A2 associates with poor survival of nasopharyngeal carcinoma patients treated with induction chemotherapy.
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Huang PY, Zeng TT, Ban X, Li MQ, Zhang BZ, Zhu YH, Hua WF, Mai HQ, Zhang L, Guan XY, and Li Y
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- Adult, Aged, Biomarkers, Tumor genetics, Carcinoma genetics, Cell Line, Tumor, Cell Movement genetics, Cell Proliferation, Chemoradiotherapy methods, Cisplatin therapeutic use, Female, Fluorouracil therapeutic use, Humans, Male, Middle Aged, Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms genetics, Peptide Initiation Factors genetics, RNA Interference, RNA, Small Interfering genetics, RNA-Binding Proteins genetics, Young Adult, Eukaryotic Translation Initiation Factor 5A, Carcinoma drug therapy, Carcinoma mortality, Induction Chemotherapy methods, Nasopharyngeal Neoplasms drug therapy, Nasopharyngeal Neoplasms mortality, Peptide Initiation Factors biosynthesis, RNA-Binding Proteins biosynthesis
- Abstract
Background: Nasopharyngeal carcinoma (NPC) is a type of head-neck cancer with a distinguishable geographic and racial distribution worldwide. Increasing evidence supports that the accumulation of additional genetic and epigenetic abnormalities is important in driving the NPC tumorigenic process. In this study, we aim to investigate the association between EIF5A2 (Eukaryotic translation initiation factor 5A2) expression status and NPC clinical outcomes., Methods: The expression status of EIF5A2 was investigated in the NPC tissue microarray. Tissues were from 166 NPC patients staging II-IV, collected between 1999 and 2005. All patients were administered 2-3 cycles of DDP (cisplatin) + 5-Fu (5-fluorouracil) induction therapy and then treated with a uniform conventional two-dimensional radiotherapy. Cell motility assay, tumor growth assay and cytotoxicity assay were performed on the EIF5A2 overexpressed cells and control cells. siRNA was also used in the in vitro studies., Results: Positive staining of EIF5A2 was observed in 85.4 % (105/123) informative tumor cases. Multivariate analyses demonstrated that EIF5A2 was an independent prognostic marker of poor overall survival (OS) (P = 0.041), failure-free survival (FFS) (P = 0.029), and distant failure-free survival (D-FFS) (P = 0.043) in patients with locoregionally advanced NPC patients treated with cisplatin + 5-Fu chemoradiotherapy. The forced expression of EIF5A2 in NPC cells enhanced the cells' motility and growth ability. Knock-down of EIF5A2 in NPC cells decreased the cell's motility and growth ability. Our results also demonstrated that EIF5A2 overexpression induced chemoresistance of NPC cells to 5-Fu., Conclusions: Our findings suggested that EIF5A2 expression, as examined by immunohistochemistry, could function as an independent prognostic factor of outcomes in NPC patients with cisplatin + 5-Fu chemoradiotherapy. EIF5A2 might be a novel therapeutic target for the inhibition of NPC progress.
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- 2016
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17. CD133+ liver cancer stem cells resist interferon-gamma-induced autophagy.
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Li J, Chen JN, Zeng TT, He F, Chen SP, Ma S, Bi J, Zhu XF, and Guan XY
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- AC133 Antigen, Animals, Antigens, CD biosynthesis, Autophagy drug effects, Carcinoma, Hepatocellular pathology, Cell Line, Tumor, Cell Proliferation drug effects, Cell Proliferation genetics, Gene Expression Regulation, Neoplastic drug effects, Glycoproteins biosynthesis, Humans, Interferon-gamma administration & dosage, Liver Neoplasms pathology, Mice, Neoplastic Stem Cells metabolism, Neoplastic Stem Cells pathology, Xenograft Model Antitumor Assays, Antigens, CD genetics, Carcinoma, Hepatocellular genetics, Glycoproteins genetics, Interferon-gamma metabolism, Liver Neoplasms genetics, Peptides genetics
- Abstract
Background: Hepatocellular carcinoma (HCC) is one of the most fatal malignancies worldwide, and CD133 is a popular cancer stem cell (CSC) marker for HCC. CD133(+) CSCs have been reported to resist conventional chemo- and radiotherapy, but little is known about their response to immune surveillance. Interferon-gamma (IFN-γ) is one of key cytokines that the immune system produce to eradicate cancer cells, so we investigated the function of IFN-γ on CD133+ HCC CSCs in this study., Methods: The response of CD133(+) cells to IFN-γ was performed with functional assays (cell proliferation assay and tumor formation in nude mice), flow cytometry, immunofluorescence staining and RNA interference., Results: We found that IFN-γ inhibited the proliferation of cell lines with low percentage of CD133(+) cells (wild-type human cells, BEL7402, QGY7701) but it did not affect the proliferation of cell lines with high percentage of CD133(+) cells (wild-type human cells, Huh7, PLC8024) in vivo and in vitro (nude mice). Flow cytometry analysis demonstrated that the percentage of CD133+ cells increased after IFN-γ treatment of low CD133(+) cell lines. Furthermore, IFN-γ induced the autophagy of low CD133(+) cell lines to decrease proliferation., Conclusion: CD133(+) HCC CSCs resisted IFN-γ-induced autophagy, which might also be a mechanism through which CSCs resist immune eradication.
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- 2016
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18. Prognostic significance of FAM3C in esophageal squamous cell carcinoma.
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Zhu YH, Zhang B, Li M, Huang P, Sun J, Fu J, and Guan XY
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- Adult, Aged, Aged, 80 and over, Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Carcinoma, Squamous Cell pathology, Esophageal Neoplasms pathology, Esophageal Squamous Cell Carcinoma, Female, Humans, Lymphatic Metastasis, Male, Middle Aged, Neoplasm Staging, Prognosis, Biomarkers, Tumor analysis, Carcinoma, Squamous Cell diagnosis, Cytokines metabolism, Epithelial-Mesenchymal Transition genetics, Esophageal Neoplasms diagnosis, Gene Expression Regulation, Neoplastic genetics, Neoplasm Proteins metabolism
- Abstract
Background: Family with sequence similarity 3, member C (FAM3C) has been identified as a novel regulator in epithelial-mesenchymal transition (EMT) and metastatic progression. However, the role of FAM3C in esophageal squamous cell carcinoma (ESCC) remains unexplored. The purpose of present study is to illustrate the role of FAM3C in predicting outcomes of patients with ESCC., Methods: FAM3C expression was measured in ESCC tissues and the matched adjacent nontumorous tissues by quantitative real-time RT-PCR and Western blot analysis. The relationship between FAM3C expression and prognosis of ESCC patients was further evaluated by univariate and multivariate regression analyses. Univariate and multivariate analyses of the prognostic factors were performed using Cox proportional hazards model., Results: The FAM3C mRNA expression was remarkably upregulated in ESCC compared with their nontumor counterparts (P < 0.001). In addition, high expression of FAM3C was significantly associated with pT stage (P = 0.014) , pN stage (P = 0.026) and TNM stage (P = 0.003). Kaplan-Meier analysis showed that the 7-year overall survival rate in the group with high expression of FAM3C was poorer than that in low expression group (32.0 versus 70.9 %; P < 0.001). Univariate and multivariate analyses demonstrated that FAM3C was an independent risk factor for overall survival. Moreover, Stratified analysis revealed that FAM3C expression could differentiate the prognosis of patients in early clinical stage (TNM stage I-II)., Conclusions: FAM3C expression was dramatically increased in ESCC and might serve as a valuable prognostic indicator for ESCC patients after surgery.
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- 2015
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19. ITPKA expression is a novel prognostic factor in hepatocellular carcinoma.
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Li J, Zhu YH, Huang P, Zhang B, Sun J, and Guan XY
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- Adult, Aged, Blotting, Western, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular mortality, Disease-Free Survival, Female, Humans, Kaplan-Meier Estimate, Liver Neoplasms metabolism, Liver Neoplasms mortality, Male, Middle Aged, Phosphotransferases (Alcohol Group Acceptor) analysis, Prognosis, Proportional Hazards Models, Real-Time Polymerase Chain Reaction, Biomarkers, Tumor analysis, Carcinoma, Hepatocellular pathology, Liver Neoplasms pathology, Phosphotransferases (Alcohol Group Acceptor) biosynthesis
- Abstract
Background: Inositol-1,4,5-trisphosphate-3-kinase-A (ITPKA) has recently been found to be implicated in the tumor progression of various cancers. However, the expression and the prognostic value of ITPKA in hepatocellular carcinoma (HCC) remains unexplored. The aim of this study is to investigate the clinical significance of ITPKA expression in HCC., Methods: We determined the expression level of ITPKA in 135 cases of HCC tissues and the matched adjacent nontumorous tissues by quantitative real-time RT-PCR. The correlation between ITPKA expression and prognosis of HCC patients was further evaluated by univariate and multivariate analysis. Multivariate analysis of the prognostic factors was performed with Cox proportional hazards model., Results: Up-regulation of ITPKA occurred in 48.9% of primary HCCs compared with their nontumor counterparts (P < 0.001). In addition, high expression of ITPKA was significantly associated with vascular invasion (P = 0.001) and TNM stage (P = 0.005). Kaplan-Meier analysis showed that the 5-year overall survival (OS) and relapse-free survival (RFS) rate in the group with high expression of ITPKA is poorer than that in low expression group (32.2 and 26.8% versus 59.2 and 57.7%). Univariate and multivariate analyses revealed that ITPKA was an independent prognostic factor for OS and RFS. Moreover, Stratified analysis revealed that its prognostic significance still existed within the subgroup of patients with early clinical stage (TNM stage I) or normal serum AFP level (≤25 μg/L)., Conclusion: Our data indicated that ITPKA expression was significantly up-regulated in HCC and could serve as a potential novel prognostic biomarker for HCC patients after surgery.
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- 2015
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20. miR-31 is consistently inactivated in EBV-associated nasopharyngeal carcinoma and contributes to its tumorigenesis.
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Cheung CC, Chung GT, Lun SW, To KF, Choy KW, Lau KM, Siu SP, Guan XY, Ngan RK, Yip TT, Busson P, Tsao SW, and Lo KW
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- Carcinogenesis genetics, Carcinoma, Cell Movement genetics, Cell Proliferation, Cell Survival genetics, Comparative Genomic Hybridization, DNA Methylation genetics, Down-Regulation genetics, Gene Deletion, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Homozygote, Humans, MicroRNAs genetics, Minichromosome Maintenance Complex Component 2 metabolism, Mixed Function Oxygenases metabolism, Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms pathology, Phosphorylation, Promoter Regions, Genetic, Repressor Proteins metabolism, Tumor Suppressor Protein p53 metabolism, Carcinogenesis pathology, Herpesvirus 4, Human physiology, MicroRNAs metabolism, Nasopharyngeal Neoplasms genetics, Nasopharyngeal Neoplasms virology
- Abstract
Background: As a distinctive type of head and neck cancers, nasopharyngeal carcinoma (NPC) is genesis from the clonal Epstein-Barr virus (EBV)-infected nasopharyngeal epithelial cells accumulated with multiple genetic lesions. Among the recurrent genetic alterations defined, loss of 9p21.3 is the most frequent early event in the tumorigenesis of EBV-associated NPC. In addition to the reported CDKN2A/p16, herein, we elucidated the role of a miRNA, miR-31 within this 9p21.3 region as NPC-associated tumor suppressor., Methods: The expression and promoter methylation of miR-31 were assessed in a panel of NPC tumor lines and primary tumors. Its in vitro and in vivo tumor suppression function was investigated through the ectopic expression of miR-31 in NPC cells. We also determined the miR-31 targeted genes and its involvement in the growth in NPC., Results: Downregulation of miR-31 expression was detected in almost all NPC cell line, patient-derived xenografts (PDXs) and primary tumors. Both homozygous deletion and promoter hypermethylation were shown to be major mechanisms for miR-31 silencing in this cancer. Strikingly, loss of miR-31 was also obviously observed in the dysplastic lesions of nasopharynx. Restoration of miR-31 in C666-1 cells inhibited the cell proliferation, colony-forming and migratory capacities. Dramatic reduction of in vitro anchorage-independent growth and in vivo tumorigenic potential were demonstrated in the stable clones expressing miR-31. Furthermore, we proved that miR-31 suppressed the NPC cell growth via targeting FIH1 and MCM2., Conclusions: The findings provide strong evidence to support miR-31 as a new NPC-associated tumor suppressor on 9p21.3 region. The inactivation of miR-31 may contribute to the early development of NPC.
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- 2014
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21. Tumor suppressor genes on frequently deleted chromosome 3p in nasopharyngeal carcinoma.
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Chen J, Fu L, Zhang LY, Kwong DL, Yan L, and Guan XY
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- Cell Adhesion Molecules genetics, Cytoskeletal Proteins, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Heterotrimeric GTP-Binding Proteins genetics, Humans, RNA-Binding Proteins genetics, Trans-Activators genetics, Transducin, Chromosome Deletion, Chromosomes, Human, Pair 3 genetics, Genes, Tumor Suppressor, Nasopharyngeal Neoplasms genetics, Tumor Suppressor Proteins genetics
- Abstract
Nasopharyngeal carcinoma (NPC) is among the most common malignancies in southern China. Deletion of genomic DNA, which occurs during the complex pathogenesis process for NPC, represents a pivotal mechanism in the inactivation of tumor suppressor genes (TSGs). In many circumstances, loss of TSGs can be detected as diagnostic and prognostic markers in cancer. The short arm of chromosome 3 (3p) is a frequently deleted chromosomal region in NPC, with 3p21.1-21.2 and 3p25.2-26.1 being the most frequently deleted minimal regions. In recent years, our research group and others have focused on the identification and characterization of novel target TSGs at 3p, such as RASSF1A, BLU, RBMS3, and CHL1, in the development and progression of NPC. In this review, we summarize recent findings of TSGs at 3p and discuss some of these genes in detail. A better understanding of TSGs at 3p will significantly improve our understanding of NPC pathogenesis, diagnosis, and treatment.
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- 2012
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22. Overexpression of eIF-5A2 in mice causes accelerated organismal aging by increasing chromosome instability.
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Chen M, Huang JD, Deng HK, Dong S, Deng W, Tsang SL, Huen MS, Chen L, Zan T, Zhu GX, and Guan XY
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- Animals, Bone and Bones diagnostic imaging, Bone and Bones pathology, Cell Transformation, Neoplastic genetics, Cellular Senescence genetics, Female, Gene Expression Regulation, Developmental, Male, Mice, Mice, Transgenic, Phenotype, Pregnancy, Radiography, Aging genetics, Chromosomal Instability genetics, Gene Expression genetics, Peptide Initiation Factors genetics, Peptide Initiation Factors metabolism
- Abstract
Background: Amplification of 3q26 is one of the most frequent genetic alterations in many human malignancies. Recently, we isolated a novel oncogene eIF-5A2 within the 3q26 region. Functional study has demonstrated the oncogenic role of eIF-5A2 in the initiation and progression of human cancers. In the present study, we aim to investigate the physiological and pathological effect of eIF-5A2 in an eIF-5A2 transgenic mouse model., Methods: An eIF-5A2 transgenic mouse model was generated using human eIF-5A2 cDNA. The eIF-5A2 transgenic mice were characterized by histological and immunohistochemistry analyses. The aging phenotypes were further characterized by wound healing, bone X-ray imaging and calcification analysis. Mouse embryo fibroblasts (MEF) were isolated to further investigate molecular mechanism of eIF-5A2 in aging., Results: Instead of resulting in spontaneous tumor formation, overexpression of eIF-5A2 accelerated the aging process in adult transgenic mice. This included decreased growth rate and body weight, shortened life span, kyphosis, osteoporosis, delay of wound healing and ossification. Investigation of the correlation between cellular senescence and aging showed that cellular senescence is not required for the aging phenotypes in eIF-5A2 mice. Interestingly, we found that activation of eIF-5A2 repressed p19 level and therefore destabilized p53 in transgenic mouse embryo fibroblast (MEF) cells. This subsequently allowed for the accumulation of chromosomal instability, such as errors in cell dividing during metaphase and anaphase. Additionally, a significantly increase in number of aneuploidy cells (p < 0.05) resulted from an increase in the incidences of misaligned and lagging chromosomal materials, anaphase bridges, and micronuclei in the transgenic mice., Conclusion: These observations suggest that eIF-5A2 mouse models could accelerate organismal aging by increasing chromosome instability.
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- 2011
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23. Overexpression of GPR39 contributes to malignant development of human esophageal squamous cell carcinoma.
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Xie F, Liu H, Zhu YH, Qin YR, Dai Y, Zeng T, Chen L, Nie C, Tang H, Li Y, Fu L, and Guan XY
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- Animals, Carcinoma, Squamous Cell metabolism, Carcinoma, Squamous Cell pathology, Cell Line, Tumor, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic metabolism, Cell Transformation, Neoplastic pathology, Esophageal Neoplasms metabolism, Esophageal Neoplasms pathology, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Mice, Mice, Nude, Microarray Analysis, Receptors, G-Protein-Coupled metabolism, Receptors, G-Protein-Coupled physiology, Tissue Array Analysis, Transplantation, Heterologous, Up-Regulation genetics, Up-Regulation physiology, Carcinoma, Squamous Cell genetics, Esophageal Neoplasms genetics, Receptors, G-Protein-Coupled genetics
- Abstract
Background: By using cDNA microarray analysis, we identified a G protein-coupled receptor, GPR39, that is significantly up-regulated in ESCC. The aim of this study is to investigate the role of GPR39 in human esophageal cancer development, and to examine the prevalence and clinical significance of GPR39 overexpression in ESCC., Methods: The mRNA expression level of GPR39 was analyzed in 9 ESCC cell lines and 50 primary ESCC tumors using semi-quantitative RT-PCR. Immunohistochemistry was used to assess GPR39 protein expression in tissue arrays containing 300 primary ESCC cases. In vitro and in vivo studies were done to elucidate the tumorigenic role of GPR39 in ESCC cells., Results: We found that GPR39 was frequently overexpressed in primary ESCCs in both mRNA level (27/50, 54%) and protein level (121/207, 58.5%), which was significantly associated with the lymph node metastasis and advanced TNM stage (P < 0.01). Functional studies showed that GPR39 has a strong tumorigenic ability. Introduction of GPR39 gene into ESCC cell line KYSE30 could promote cell proliferation, increase foci formation, colony formation in soft agar, and tumor formation in nude mice. The mechanism by which amplified GPR39 induces tumorigenesis was associated with its role in promoting G1/S transition via up-regulation of cyclin D1 and CDK6. Further study found GPR39 could enhance cell motility and invasiveness by inducing EMT and remodeling cytoskeleton. Moreover, depletion of endogenous GPR39 by siRNA could effectively decrease the oncogenicity of ESCC cells., Conclusions: The present study suggests that GPR39 plays an important tumorigenic role in the development and progression of ESCC.
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- 2011
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24. Intensive expression of Bmi-1 is a new independent predictor of poor outcome in patients with ovarian carcinoma.
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Yang GF, He WP, Cai MY, He LR, Luo JH, Deng HX, Guan XY, Zeng MS, Zeng YX, and Xie D
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- Biomarkers, Tumor genetics, Cyclin-Dependent Kinase Inhibitor p16 biosynthesis, Female, Gene Amplification, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Middle Aged, Nuclear Proteins genetics, Ovarian Neoplasms genetics, Ovarian Neoplasms pathology, Polycomb Repressive Complex 1, Prognosis, Proto-Oncogene Proteins genetics, Repressor Proteins genetics, Treatment Outcome, Tumor Suppressor Protein p14ARF biosynthesis, Biomarkers, Tumor biosynthesis, Nuclear Proteins biosynthesis, Ovarian Neoplasms metabolism, Proto-Oncogene Proteins biosynthesis, Repressor Proteins biosynthesis
- Abstract
Background: It has been suggested that the B-cell specific moloney leukemia virus insertion site 1 (Bmi-1) gene plays an oncogenic role in several types of human cancer, but the status of Bmi-1 amplification and expression in ovarian cancer and its clinical/prognostic significance are unclear., Methods: The methods of immunohistochemistry and fluorescence in situ hybridization were utilized to examine protein expression and amplification of Bmi-1 in 30 normal ovaries, 30 ovarian cystadenomas, 40 borderline ovarian tumors and 179 ovarian carcinomas., Results: Intensive expression of Bmi-1 was detected in none of the normal ovaries, 3% cystadenomas, 10% borderline tumors, and 37% ovarian carcinomas, respectively. Amplification of Bmi-1 was detected in 8% of ovarian carcinomas. In ovarian carcinomas, significant positive associations were found between intensive expression of Bmi-1 and the tumors ascending histological grade, later pT/pN/pM and FIGO stages (P < 0.05). In univariate survival analysis of the ovarian carcinoma cohorts, a significant association of intensive expression of Bmi-1 with shortened patient survival (mean 49.3 months versus 100.3 months, p < 0.001) was demonstrated. Importantly, Bmi-1 expression provided significant independent prognostic parameters in multivariate analysis (p = 0.005)., Conclusions: These findings provide evidence that intensive expression of Bmi-1 might be important in the acquisition of an invasive and/or aggressive phenotype of ovarian carcinoma, and serve as a independent biomarker for shortened survival time of patients.
- Published
- 2010
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