9 results on '"Ban, Xiaojiao"'
Search Results
2. Down‐regulation of POTEG predicts poor prognosis in esophageal squamous cell carcinoma patients.
- Author
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Wang, Ling, Li, Mengqing, Zhan, Yuting, Ban, Xiaojiao, Zeng, Tingting, Zhu, Yinghui, Yun, Jingping, Guan, Xin‐Yuan, and Li, Yan
- Published
- 2018
- Full Text
- View/download PDF
3. Expression of EIF5A2 associates with poor survival of nasopharyngeal carcinoma patients treated with induction chemotherapy.
- Author
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Pei-Yu Huang, Ting-Ting Zeng, Xiaojiao Ban, Meng-Qing Li, Bao-Zhu Zhang, Ying-Hui Zhu, Wen-Feng Hua, Hai-Qiang Mai, Li Zhang, Xin-Yuan Guan, Yan Li, Huang, Pei-Yu, Zeng, Ting-Ting, Ban, Xiaojiao, Li, Meng-Qing, Zhang, Bao-Zhu, Zhu, Ying-Hui, Hua, Wen-Feng, Mai, Hai-Qiang, and Zhang, Li
- Subjects
NASOPHARYNX cancer ,HEAD & neck cancer ,CANCER chemotherapy ,INITIATION factors (Biochemistry) ,MICROARRAY technology ,EPIGENETICS ,GENETICS ,CANCER-related mortality ,CISPLATIN ,FLUOROURACIL ,CANCER ,CELL lines ,CELL physiology ,CELL motility ,GENES ,NASOPHARYNX tumors ,PROTEINS ,RNA - 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. [ABSTRACT FROM AUTHOR]- Published
- 2016
- Full Text
- View/download PDF
4. Increased Expression of EIF5A2, Via Hypoxia or Gene Amplification, Contributes to Metastasis and Angiogenesis of Esophageal Squamous Cell Carcinoma.
- Author
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Li, Yan, Fu, Li, Li, Jian-Biao, Qin, Yanru, Zeng, Ting-ting, Zhou, Jie, Zeng, Zhao-Lei, Chen, Jinna, Cao, Ting-Ting, Ban, Xiaojiao, Qian, Chaonan, Cai, Zongwei, Xie, Dan, Huang, Peng, and Guan, Xin-Yuan
- Abstract
Background & Aims: Solid tumors often become hypoxic, leading to activation of hypoxia-response genes. We investigated the effects of overexpression of the hypoxia response genes eIF5A2 in esophageal squamous cell carcinoma (ESCC). Methods: We used quantitative real-time polymerase chain reaction and immunohistochemistry analyses to compare expression of eIF5A2 between paired ESCC samples and nontumor esophageal tissues, and fluorescence in situ hybridization to detect gene copy-number alterations. Luciferase reporter and chromatin immunoprecipitation assays were used to study interactions between eIF5A2 and hypoxia-inducible factor-1α (HIF1α). We determined the effects of eIF5A2 overexpression and knockdown in ESCC cell lines and growth of ESCC xenograft tumors in nude mice. Results: Levels of eIF5A2 messenger RNA and protein were increased in >40% of ESCC samples compared with matched nontumor tissues, along with levels of HIF1α and vascular endothelial growth factor. Increased levels of EIF5A2 were significantly associated with ESCC metastasis to lymph nodes (P < .001) and tissue invasion (P = .037), and shorter survival times of patients (P < .001). Amplification of eIF5A2 was detected in 35.14% of ESCC samples that overexpressed eIF5A2. Hypoxia increased expression of eIF5A2 4- to 8-fold in ESCC cell lines; we observed bidirectional regulation between eIF5A2 and HIF1α. Transient transfection of ESCC cell lines with eIF5A2 increased their migratory and invasive abilities and markers of the epithelial to mesenchymal transition, and eIF5A2 knockdown or HIFα inhibition reduced these. In mice, xenograft tumors grown from ESCC cells that expressed eIF5A2 formed tumors more rapidly than cells that expressed only vector (controls); they also expressed higher levels of HIF1α and vascular endothelial growth factor, and formed more microvessels than controls. Knockdown of eIF5A2 in ESCC cells with interfering RNAs reduced their growth as xenograft tumors in mice, particularly when mice were given docetaxel or cisplatin. Conclusions: eIF5A2 is overexpressed by gene amplification or hypoxia in ESCCs, and associated with up-regulation of HIF1α, metastasis, and shorter survival times of patients. Increased expression of eIF5A2 increases metastasis and angiogenesis in ESCC via the HIF1α-mediated signaling pathway. [Copyright &y& Elsevier]
- Published
- 2014
- Full Text
- View/download PDF
5. Characterization of Tumor Suppressive Function of cornulin in Esophageal Squamous Cell Carcinoma.
- Author
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Chen, Kai, Li, Yan, Dai, Yongdong, Li, Jiangchao, Qin, Yanru, Zhu, Yinghui, Zeng, Tingting, Ban, Xiaojiao, Fu, Li, and Guan, Xin-Yuan
- Subjects
TUMOR suppressor genes ,ESOPHAGEAL cancer ,DNA microarrays ,MESSENGER RNA ,LYMPH node cancer ,RNA interference ,CANCER-related mortality ,GENE silencing ,PROGNOSIS - Abstract
By using cDNA microarray analysis, we identified cornulin (CRNN) gene was frequently downregulated in esophageal squamous cell carcinoma (ESCC). In the present study, we investigated the role of CRNN in ESCC development. The results showed that CRNN was frequently downregulated in primary ESCCs in both mRNA level (26/56, 46.4%) and protein level (137/249, 55%), which was significantly associated with lymph node metastases (P=0.027), advanced clinical stage (P=0.039), and overall survival rate (P<0.001). Multivariate analysis indicated that the CRNN downregulation was an independent prognostic factor for ESCC. Functional studies with both in vitro and in vivo assays demonstrated that CRNN had strong tumor suppressive ability in ESCC cells. The tumor-suppressive mechanism of CRNN was associated with its role in cell cycle arrest at G1/S checkpoint by upregulating expressions of P21
WAF1/CIP1 and Rb. Silencing CRNN expression by RNA interference could effectively inhibit its tumor suppressive effect. In conclusion, our findings demonstrate that CRNN is a tumor suppressor gene that plays a critical tumor suppressive role in ESCC. [ABSTRACT FROM AUTHOR]- Published
- 2013
- Full Text
- View/download PDF
6. PDSS2 Deficiency Induces Hepatocarcinogenesis by Decreasing Mitochondrial Respiration and Reprogramming Glucose Metabolism.
- Author
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Li Y, Lin S, Li L, Tang Z, Hu Y, Ban X, Zeng T, Zhou Y, Zhu Y, Gao S, Deng W, Zhang X, Xie D, Yuan Y, Huang P, Li J, Cai Z, and Guan XY
- Subjects
- Animals, Biomarkers, Tumor genetics, Carcinogenesis genetics, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Cellular Reprogramming genetics, Gene Expression Regulation, Neoplastic, Glucose metabolism, Glycolysis genetics, Humans, Liver metabolism, Liver pathology, Liver Neoplasms metabolism, Liver Neoplasms pathology, Mice, Mitochondria metabolism, Mitochondria pathology, Nitric Oxide Synthase genetics, Xenograft Model Antitumor Assays, Alkyl and Aryl Transferases genetics, Carcinoma, Hepatocellular genetics, Liver Neoplasms genetics, Mitochondria genetics
- Abstract
Glucose metabolic reprogramming from oxidative phosphorylation to glycolysis is one of the hallmarks of cancer development. Coenzyme Q10 (CoQ10) is essential for electron transport in the mitochondrial respiratory chain and for antioxidant defense. Here, we investigated the role of a key factor in CoQ10 synthesis, prenyldiphosphate synthase subunit 2 ( PDSS2 ), in hepatocellular carcinoma (HCC) tumorigenesis. PDSS2 was frequently downregulated in HCC tissues and was significantly associated with poorer HCC prognosis ( P = 0.027). PDSS2 downregulation was a prognostic factor independent of T status and stage ( P = 0.028). Downregulation of CoQ10 was significantly correlated with downregulation of PDSS2 in HCC tumor tissues ( R = 0.414; P < 0.001). Of the six different splicing isoforms of PDSS2, the five variants other than full-length PDSS2 showed loss of function in HCC. Reintroduction of full-length PDSS2 into HCC cells increased CoQ10 and mitochondrial electron transport complex I activity and subsequently induced a metabolic shift from aerobic glycolysis to mitochondrial respiration in cells. Reintroduction of PDSS2 also inhibited foci formation, colony formation in soft agar, and tumor formation in nude mice. Knockdown of PDSS2 induced chromosomal instability in the MIHA immortalized human liver cell line. Furthermore, knockdown of PDSS2 in MIHA induced malignant transformation. Overall, our findings indicate that PDSS2 deficiency might be a novel driving factor in HCC development. Significance: Downregulation of PDSS2 is a driving factor in hepatocellular carcinoma tumorigenesis. Cancer Res; 78(16); 4471-81. ©2018 AACR ., (©2018 American Association for Cancer Research.)
- Published
- 2018
- Full Text
- View/download PDF
7. Expression of EIF5A2 associates with poor survival of nasopharyngeal carcinoma patients treated with induction chemotherapy.
- Author
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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
- Subjects
- 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.
- Published
- 2016
- Full Text
- View/download PDF
8. Stemness and chemotherapeutic drug resistance induced by EIF5A2 overexpression in esophageal squamous cell carcinoma.
- Author
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Yang H, Li XD, Zhou Y, Ban X, Zeng TT, Li L, Zhang BZ, Yun J, Xie D, Guan XY, and Li Y
- Subjects
- Adult, Aged, Antineoplastic Agents pharmacology, Apoptosis drug effects, Apoptosis genetics, Blotting, Western, Carcinoma, Squamous Cell drug therapy, Carcinoma, Squamous Cell surgery, Cell Line, Tumor, Docetaxel, Drug Resistance, Neoplasm drug effects, Esophageal Neoplasms drug therapy, Esophageal Neoplasms surgery, Female, Fluorouracil pharmacology, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Male, Middle Aged, Neoplastic Stem Cells drug effects, Paclitaxel pharmacology, Peptide Initiation Factors metabolism, RNA-Binding Proteins metabolism, Retrospective Studies, Reverse Transcriptase Polymerase Chain Reaction, Taxoids pharmacology, Eukaryotic Translation Initiation Factor 5A, Carcinoma, Squamous Cell genetics, Drug Resistance, Neoplasm genetics, Esophageal Neoplasms genetics, Gene Expression Regulation, Neoplastic, Neoplastic Stem Cells metabolism, Peptide Initiation Factors genetics, RNA-Binding Proteins genetics
- Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies of the digestive tract in East Asian countries. Multimodal therapies, including adjuvant chemotherapy and neo-adjuvant chemotherapy, have become more often used for patients with advanced ESCC. However, the chemotherapy effect is often limited by patients' drug resistance. This study demonstrated that EIF5A2 (eukaryotic translation initiation factor 5A2) overexpression induced stemness and chemoresistance in ESCC cells. We showed that EIF5A2 overexpression in ESCC cells resulted in increased chemoresistance to 5-fluorouracil (5-FU), docetaxel and taxol. In contrast, shRNAs suppressing eIF5A2 increased tumor sensitivity to these chemotherapeutic drugs. In addition, EIF5A2 overexpression was correlated with a poorer overall survival in patients with ESCC who underwent taxane-based chemotherapy after esophagectomy (P < 0.05). Based on these results, we suggest that EIF5A2 could be a predictive biomarker for selecting appropriate chemo-treatment for ESCC patients and EIF5A2 inhibitors might be considered as combination therapy to enhance chemosensitivity in patients with ESCC.
- Published
- 2015
- Full Text
- View/download PDF
9. Characterization of tumor suppressive function of cornulin in esophageal squamous cell carcinoma.
- Author
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Chen K, Li Y, Dai Y, Li J, Qin Y, Zhu Y, Zeng T, Ban X, Fu L, and Guan XY
- Subjects
- Animals, Blotting, Western, Carcinoma, Squamous Cell genetics, Cell Cycle genetics, Cell Cycle Checkpoints genetics, Cell Cycle Checkpoints physiology, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p21 genetics, Cyclin-Dependent Kinase Inhibitor p21 metabolism, Esophageal Neoplasms genetics, Esophageal Squamous Cell Carcinoma, Humans, Immunohistochemistry, In Vitro Techniques, Membrane Proteins genetics, Mice, Mice, Nude, Neoplasm Proteins genetics, RNA Interference, Retinoblastoma Protein genetics, Retinoblastoma Protein metabolism, Reverse Transcriptase Polymerase Chain Reaction, Tissue Array Analysis, Carcinoma, Squamous Cell metabolism, Cell Cycle physiology, Esophageal Neoplasms metabolism, Membrane Proteins metabolism, Neoplasm Proteins metabolism
- Abstract
By using cDNA microarray analysis, we identified cornulin (CRNN) gene was frequently downregulated in esophageal squamous cell carcinoma (ESCC). In the present study, we investigated the role of CRNN in ESCC development. The results showed that CRNN was frequently downregulated in primary ESCCs in both mRNA level (26/56, 46.4%) and protein level (137/249, 55%), which was significantly associated with lymph node metastases (P=0.027), advanced clinical stage (P=0.039), and overall survival rate (P<0.001). Multivariate analysis indicated that the CRNN downregulation was an independent prognostic factor for ESCC. Functional studies with both in vitro and in vivo assays demonstrated that CRNN had strong tumor suppressive ability in ESCC cells. The tumor-suppressive mechanism of CRNN was associated with its role in cell cycle arrest at G1/S checkpoint by upregulating expressions of P21(WAF1/CIP1) and Rb. Silencing CRNN expression by RNA interference could effectively inhibit its tumor suppressive effect. In conclusion, our findings demonstrate that CRNN is a tumor suppressor gene that plays a critical tumor suppressive role in ESCC.
- Published
- 2013
- Full Text
- View/download PDF
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