The Experts below are selected from a list of 1762032 Experts worldwide ranked by ideXlab platform
Pin-i Huang - One of the best experts on this subject based on the ideXlab platform.
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epithelial mesenchymal transition transcription factor zeb1 zeb2 co expression predicts poor prognosis and maintains tumor initiating properties in head and neck cancer
Oral Oncology, 2013Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
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Epithelial-mesenchymal transition transcription factor ZEB1/ZEB2 co-expression predicts poor prognosis and maintains tumor-initiating properties in head and neck cancer
Oral oncology, 2012Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
Pen Yuan Chu - One of the best experts on this subject based on the ideXlab platform.
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epithelial mesenchymal transition transcription factor zeb1 zeb2 co expression predicts poor prognosis and maintains tumor initiating properties in head and neck cancer
Oral Oncology, 2013Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
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Epithelial-mesenchymal transition transcription factor ZEB1/ZEB2 co-expression predicts poor prognosis and maintains tumor-initiating properties in head and neck cancer
Oral oncology, 2012Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
Yi Wei Chen - One of the best experts on this subject based on the ideXlab platform.
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epithelial mesenchymal transition transcription factor zeb1 zeb2 co expression predicts poor prognosis and maintains tumor initiating properties in head and neck cancer
Oral Oncology, 2013Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
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Epithelial-mesenchymal transition transcription factor ZEB1/ZEB2 co-expression predicts poor prognosis and maintains tumor-initiating properties in head and neck cancer
Oral oncology, 2012Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
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oct 4 expression maintained cancer stem like properties in lung cancer derived CD133 positive cells
PLOS ONE, 2008Co-Authors: Yuchih Chen, Yi Wei Chen, Hanshui Hsu, Tunghu Tsai, Chorngkuang How, Chienying WangAbstract:CD133 (prominin-1), a 5-transmembrane glycoprotein, has recently been considered to be an important marker that represents the subset population of cancer stem-like cells. Herein we report the isolation of CD133-positive cells (LC-CD133+) and CD133-negative cells (LC-CD133−) from tissue samples of ten patients with non-small cell lung cancer (LC) and five LC cell lines. LC-CD133+ displayed higher Oct-4 expressions with the ability to self-renew and may represent a reservoir with proliferative potential for generating lung cancer cells. Furthermore, LC-CD133+, unlike LC-CD133−, highly co-expressed the multiple drug-resistant marker ABCG2 and showed significant resistance to chemotherapy agents (i.e., cisplatin, etoposide, doxorubicin, and paclitaxel) and radiotherapy. The treatment of Oct-4 siRNA with lentiviral vector can specifically block the capability of LC-CD133+ to form spheres and can further facilitate LC-CD133+ to differentiate into LC-CD133−. In addition, knock-down of Oct-4 expression in LC-CD133+ can significantly inhibit the abilities of tumor invasion and colony formation, and increase apoptotic activities of caspase 3 and poly (ADP-ribose) polymerase (PARP). Finally, in vitro and in vivo studies further confirm that the treatment effect of chemoradiotherapy for LC-CD133+ can be improved by the treatment of Oct-4 siRNA. In conclusion, we demonstrated that Oct-4 expression plays a crucial role in maintaining the self-renewing, cancer stem-like, and chemoradioresistant properties of LC-CD133+. Future research is warranted regarding the up-regulated expression of Oct-4 in LC-CD133+ and malignant lung cancer.
Lo Lin Tsai - One of the best experts on this subject based on the ideXlab platform.
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epithelial mesenchymal transition transcription factor zeb1 zeb2 co expression predicts poor prognosis and maintains tumor initiating properties in head and neck cancer
Oral Oncology, 2013Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
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Epithelial-mesenchymal transition transcription factor ZEB1/ZEB2 co-expression predicts poor prognosis and maintains tumor-initiating properties in head and neck cancer
Oral oncology, 2012Co-Authors: Pen Yuan Chu, Lo Lin Tsai, Yi Wei Chen, Pin-i HuangAbstract:Summary Objectives Both epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties may be involved in metastasis, which contributes to the high mortality rate of patients with head and neck cancers (HNCs). However, the mechanisms through which the EMT transcription factors ZEB1 and ZEB2 regulate HNC are still unclear. Methods Tumor initiating capability of HNC-CH133 + cells with ZEB1/2 knockdown or co-overexpression was presented in vitro and in vivo. Results In the present study, we demonstrated that ZEB1/ZEB2 expression was significantly increased in HNC-CD133 + CSC-like cells compared with HNC-CD133 − cells. The small interfering RNA (siRNA)-mediated co-knockdown of ZEB1 and ZEB2 (siZEB1/2) in HNC-CH133 + cells suppressed their CSC-like properties, including self-renewal ability, the expression of stemness markers, and drug resistance. In contrast, the co-overexpression of ZEB1/ZEB2 in HNC-CD133 − cells enhanced their sphere-forming ability and increased the percentage of CD44-positive cells and side population cells. In vivo studies showed that the delivery of siZEB1/2 to xenograft tumors in nude mice reduced tumor growth and the rate of distant metastasis. In clinical samples, the levels of ZEB1/ZEB2 expression were low in local lesions but high in metastatic lymph nodes in HNC tissues. Patients with tumors that co-expressed ZEB1 high and ZEB2 high had especially poor survival rates. Conclusion Therapies targeting ZEB1/ZEB2 in HNC-CD133 + cells may provide a new approach for HNC therapy in the future.
Giovanni Camussi - One of the best experts on this subject based on the ideXlab platform.
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Role of CD133 Molecule in Wnt Response and Renal Repair.
Stem cells translational medicine, 2018Co-Authors: Alessia Brossa, Elli Papadimitriou, Federica Collino, Danny Incarnato, Salvatore Oliviero, Giovanni Camussi, Benedetta BussolatiAbstract:Renal repair after injury is dependent on clonal expansion of proliferation-competent cells. In the human kidney, the expression of CD133 characterizes a population of resident scattered cells with resistance to damage and ability to proliferate. However, the biological function of the CD133 molecule is unknown. By RNA sequencing, we found that cells undergoing cisplatin damage lost the CD133 signature and acquired metanephric mesenchymal and regenerative genes such as SNAIL1, KLF4, SOX9, and WNT3. CD133 was reacquired in the recovery phase. In CD133-Kd cells, lack of CD133 limited cell proliferation after injury and was specifically correlated with deregulation of Wnt signaling and E-cadherin pathway. By immunoprecipitation, CD133 appeared to form a complex with E-cadherin and β-catenin. In parallel, CD133-Kd cells showed lower β-catenin levels in basal condition and after Wnt pathway activation and reduced TCF/LEF promoter activation in respect to CD133+ cells. Finally, the lack of CD133 impaired generation of nephrospheres while favoring senescence. These data indicate that CD133 may act as a permissive factor for β-catenin signaling, preventing its degradation in the cytoplasm. Therefore, CD133 itself appears to play a functional role in renal tubular repair through maintenance of proliferative response and control of senescence. Stem Cells Translational Medicine 2018;7:283-294.
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CD133 + cells as a therapeutic target for kidney diseases
Expert opinion on therapeutic targets, 2012Co-Authors: Benedetta Bussolati, Federica Collino, Giovanni CamussiAbstract:The availability of antibodies recognizing the glycosylation-dependent expression of AC133 epitope of CD133 allowed the identification of stem cells in different human tissues. In the kidney, CD133 has been identified as a marker of progenitor cells within the nephron, both in the cortex and in the inner medulla, showing features of non-differentiated mesenchymal progenitors. In addition, CD133 may be considered a marker of renal repair, as the hypoxic microenvironment occurring after injury may favor the acquirement of CD133 progenitor properties by cells of the nephron. Areas covered in this review include CD133 expression that, in renal pathology, has been related to excessive proliferation and/or reduced differentiation of renal progenitors, which occurs in polycystic kidney disease and glomerular diseases. Also included are data from literature, which by contrast, indicate CD133 cannot be considered a promising marker for renal cancer stem cells. CD133 could be of interest as a possible therapeutic target for nonmalignant renal pathology. Selective targeting of CD133 may allow pharmacological approaches to control proliferation or induce differentiation of CD133+ cells. In the light of a possible role of CD133 in the regulation of the anaerobic glycolytic metabolism, CD133 modulation could be of therapeutic interest in renal regeneration or diseases. Successful exploitation of CD133 will nevertheless require a better understanding of its molecular function.