6 results on '"Chang-Han Chen"'
Search Results
2. Oncogenic fibulin-5 promotes nasopharyngeal carcinoma cell metastasis through the FLJ10540/AKT pathway and correlates with poor prognosis.
- Author
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Chung-Feng Hwang, Li-Yen Shiu, Li-Jen Su, Yu-Fang Yin, Wei-Sheng Wang, Shun-Chen Huang, Tai-Jan Chiu, Chao-Cheng Huang, Yen-Yi Zhen, Hsin-Ting Tsai, Fu-Min Fang, Tai-Lin Huang, and Chang-Han Chen
- Subjects
Medicine ,Science - Abstract
BACKGROUND:Nasopharyngeal carcinoma (NPC) is known for its high metastatic potential and locoregional recurrence, although the molecular alterations that are driving NPC metastasis remain unclear at this time. This study aimed to examine the expression of fibulin-5 in NPC, correlate the results with clinicopathological variables and survival, and to investigate the role of fibulin-5 in human NPC cell lines. MATERIAL AND METHODS:Standard semi-quantitative-RT-PCR, quantitative-RT-PCR, immunoblotting, and immunohistochemistry were used to investigate the mRNA and protein expression profiles of fibulin-5 in normal and NPC tissues. Immunohistochemistry of fibulin-5 was correlated with clinicopathological characteristics by univariate analyses. NPC cells overexpressing fibulin-5 or fibulin-5-siRNA cells were generated by stable transfection to characterize the molecular mechanisms of fibulin-5-elicited cell growth and metastasis. RESULTS:Our results demonstrated that fibulin-5 overexpression in NPC specimens and significantly correlated with advanced tumor metastasis indicating a poor 5-year overall survival. Fibulin-5 was mainly expressed in the nucleus in human NPC specimens and cell lines. Functionally, fibulin-5 overexpression yielded fast growth in NPC cells. In addition, fibulin-5 promotes cell metastasis in NPC cells through increased FLJ10540 and phosphor-AKT activity. In contrast, siRNA depletion of fibulin-5 suppressed FLJ10540 expression and phosphor-AKT activity. Suppression of either fibulin-5 or FLJ10540 can cause significant inhibition with regards to cell motility in NPC cells. Finally, immunohistochemical analysis of human aggressive NPC specimens showed a significant and positive correlation between fibulin-5 and FLJ10540 expression. CONCLUSION:Higher fibulin-5 expression is not only an important indicator of poor survival, but also contributes to the development of new therapeutic strategies in the FLJ10540/AKT pathway for NPC treatment.
- Published
- 2013
- Full Text
- View/download PDF
3. VEGFA upregulates FLJ10540 and modulates migration and invasion of lung cancer via PI3K/AKT pathway.
- Author
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Chang-Han Chen, Jin-Mei Lai, Teh-Ying Chou, Cheng-Yu Chen, Li-Jen Su, Yuan-Chii Lee, Tai-Shan Cheng, Yi-Ren Hong, Chen-Kung Chou, Jacqueline Whang-Peng, Yu-Chung Wu, and Chi-Ying F Huang
- Subjects
Medicine ,Science - Abstract
BACKGROUND: Lung adenocarcinoma is the leading cause of cancer-related deaths among both men and women in the world. Despite recent advances in diagnosis and treatment, the mortality rates with an overall 5-year survival of only 15%. This high mortality is probably attributable to early metastasis. Although several well-known markers correlated with poor/metastasis prognosis in lung adenocarcinoma patients by immunohistochemistry was reported, the molecular mechanisms of lung adenocarcinoma development are still not clear. To explore novel molecular markers and their signaling pathways will be crucial for aiding in treatment of lung adenocarcinoma patients. METHODOLOGY/PRINCIPAL FINDINGS: To identify novel lung adenocarcinoma-associated /metastasis genes and to clarify the underlying molecular mechanisms of these targets in lung cancer progression, we created a bioinformatics scheme consisting of integrating three gene expression profile datasets, including pairwise lung adenocarcinoma, secondary metastatic tumors vs. benign tumors, and a series of invasive cell lines. Among the novel targets identified, FLJ10540 was overexpressed in lung cancer tissues and is associated with cell migration and invasion. Furthermore, we employed two co-expression strategies to identify in which pathway FLJ10540 was involved. Lung adenocarcinoma array profiles and tissue microarray IHC staining data showed that FLJ10540 and VEGF-A, as well as FLJ10540 and phospho-AKT exhibit positive correlations, respectively. Stimulation of lung cancer cells with VEGF-A results in an increase in FLJ10540 protein expression and enhances complex formation with PI3K. Treatment with VEGFR2 and PI3K inhibitors affects cell migration and invasion by activating the PI3K/AKT pathway. Moreover, knockdown of FLJ10540 destabilizes formation of the P110-alpha/P85-alpha-(PI3K) complex, further supporting the participation of FLJ10540 in the VEGF-A/PI3K/AKT pathway. CONCLUSIONS/SIGNIFICANCE: This finding set the stage for further testing of FLJ10540 as a new therapeutic target for treating lung cancer and may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in lung cancer cells.
- Published
- 2009
- Full Text
- View/download PDF
4. VEGFA upregulates FLJ10540 and modulates migration and invasion of lung cancer via PI3K/AKT pathway
- Author
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Li Jen Su, Cheng Yu Chen, Chi Ying F. Huang, Jin Mei Lai, Yuan Chii Lee, Jacqueline Whang-Peng, Teh Ying Chou, Yi Ren Hong, Yu Chung Wu, Chen-Kung Chou, Tai Shan Cheng, and Chang Han Chen
- Subjects
Vascular Endothelial Growth Factor A ,Pathology ,medicine.medical_specialty ,Lung Neoplasms ,lcsh:Medicine ,Cell Cycle Proteins ,Biology ,Adenocarcinoma ,Cell Biology/Cell Signaling ,Metastasis ,Phosphatidylinositol 3-Kinases ,Cell Line, Tumor ,medicine ,Adenocarcinoma of the lung ,Humans ,Neoplasm Invasiveness ,RNA, Messenger ,Neoplasm Metastasis ,RNA, Small Interfering ,Lung cancer ,lcsh:Science ,PI3K/AKT/mTOR pathway ,Oncology/Lung Cancer ,Multidisciplinary ,Lung ,Tissue microarray ,Base Sequence ,Reverse Transcriptase Polymerase Chain Reaction ,lcsh:R ,Nuclear Proteins ,Cell migration ,medicine.disease ,Up-Regulation ,Enzyme Activation ,medicine.anatomical_structure ,Microscopy, Fluorescence ,Tissue Array Analysis ,Gene Knockdown Techniques ,Cancer research ,lcsh:Q ,Proto-Oncogene Proteins c-akt ,Research Article ,Molecular Biology/Translation Mechanisms - Abstract
BACKGROUND: Lung adenocarcinoma is the leading cause of cancer-related deaths among both men and women in the world. Despite recent advances in diagnosis and treatment, the mortality rates with an overall 5-year survival of only 15%. This high mortality is probably attributable to early metastasis. Although several well-known markers correlated with poor/metastasis prognosis in lung adenocarcinoma patients by immunohistochemistry was reported, the molecular mechanisms of lung adenocarcinoma development are still not clear. To explore novel molecular markers and their signaling pathways will be crucial for aiding in treatment of lung adenocarcinoma patients. METHODOLOGY/PRINCIPAL FINDINGS: To identify novel lung adenocarcinoma-associated /metastasis genes and to clarify the underlying molecular mechanisms of these targets in lung cancer progression, we created a bioinformatics scheme consisting of integrating three gene expression profile datasets, including pairwise lung adenocarcinoma, secondary metastatic tumors vs. benign tumors, and a series of invasive cell lines. Among the novel targets identified, FLJ10540 was overexpressed in lung cancer tissues and is associated with cell migration and invasion. Furthermore, we employed two co-expression strategies to identify in which pathway FLJ10540 was involved. Lung adenocarcinoma array profiles and tissue microarray IHC staining data showed that FLJ10540 and VEGF-A, as well as FLJ10540 and phospho-AKT exhibit positive correlations, respectively. Stimulation of lung cancer cells with VEGF-A results in an increase in FLJ10540 protein expression and enhances complex formation with PI3K. Treatment with VEGFR2 and PI3K inhibitors affects cell migration and invasion by activating the PI3K/AKT pathway. Moreover, knockdown of FLJ10540 destabilizes formation of the P110-alpha/P85-alpha-(PI3K) complex, further supporting the participation of FLJ10540 in the VEGF-A/PI3K/AKT pathway. CONCLUSIONS/SIGNIFICANCE: This finding set the stage for further testing of FLJ10540 as a new therapeutic target for treating lung cancer and may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in lung cancer cells.
- Published
- 2009
5. Inhibition of Chemokine (C-C Motif) Receptor 7 Sialylation Suppresses CCL19-Stimulated Proliferation, Invasion and Anti-Anoikis
- Author
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Su, Mei-Lin, primary, Chang, Tsung-Ming, additional, Chiang, Chi-Hsiang, additional, Chang, Han-Chen, additional, Hou, Ming-Feng, additional, Li, Wen-Shan, additional, and Hung, Wen-Chun, additional
- Published
- 2014
- Full Text
- View/download PDF
6. Oncogenic Fibulin-5 Promotes Nasopharyngeal Carcinoma Cell Metastasis through the FLJ10540/AKT Pathway and Correlates with Poor Prognosis
- Author
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Shun Chen Huang, Chung Feng Hwang, Yu Fang Yin, Tai-Lin Huang, Hsin Ting Tsai, Yen Yi Zhen, Li Yen Shiu, Chao-Cheng Huang, Wei Sheng Wang, Li Jen Su, Tai Jan Chiu, Fu-Min Fang, and Chang Han Chen
- Subjects
Pathology ,medicine.medical_specialty ,Multidisciplinary ,lcsh:R ,Cell ,Nasopharyngeal neoplasm ,lcsh:Medicine ,Cell migration ,Biology ,medicine.disease ,Fibulin ,Metastasis ,stomatognathic diseases ,medicine.anatomical_structure ,Nasopharyngeal carcinoma ,otorhinolaryngologic diseases ,Cancer research ,medicine ,Carcinoma ,lcsh:Q ,lcsh:Science ,PI3K/AKT/mTOR pathway - Abstract
BACKGROUND:Nasopharyngeal carcinoma (NPC) is known for its high metastatic potential and locoregional recurrence, although the molecular alterations that are driving NPC metastasis remain unclear at this time. This study aimed to examine the expression of fibulin-5 in NPC, correlate the results with clinicopathological variables and survival, and to investigate the role of fibulin-5 in human NPC cell lines. MATERIAL AND METHODS:Standard semi-quantitative-RT-PCR, quantitative-RT-PCR, immunoblotting, and immunohistochemistry were used to investigate the mRNA and protein expression profiles of fibulin-5 in normal and NPC tissues. Immunohistochemistry of fibulin-5 was correlated with clinicopathological characteristics by univariate analyses. NPC cells overexpressing fibulin-5 or fibulin-5-siRNA cells were generated by stable transfection to characterize the molecular mechanisms of fibulin-5-elicited cell growth and metastasis. RESULTS:Our results demonstrated that fibulin-5 overexpression in NPC specimens and significantly correlated with advanced tumor metastasis indicating a poor 5-year overall survival. Fibulin-5 was mainly expressed in the nucleus in human NPC specimens and cell lines. Functionally, fibulin-5 overexpression yielded fast growth in NPC cells. In addition, fibulin-5 promotes cell metastasis in NPC cells through increased FLJ10540 and phosphor-AKT activity. In contrast, siRNA depletion of fibulin-5 suppressed FLJ10540 expression and phosphor-AKT activity. Suppression of either fibulin-5 or FLJ10540 can cause significant inhibition with regards to cell motility in NPC cells. Finally, immunohistochemical analysis of human aggressive NPC specimens showed a significant and positive correlation between fibulin-5 and FLJ10540 expression. CONCLUSION:Higher fibulin-5 expression is not only an important indicator of poor survival, but also contributes to the development of new therapeutic strategies in the FLJ10540/AKT pathway for NPC treatment.
- Published
- 2013
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