1.Influence of FOXC1 downregulating on biological behavior of nasopharyngeal carcinoma (NPC) 5-8F cell lines
Bolin CHEN ; Shijiang YI ; Peng LIU ; Lei OUYANG ; Xun LEI
The Journal of Practical Medicine 2016;32(4):527-530
Objective To investigate the Influence of FOXC1 downregulating on biological behavior of nasopharyngeal carcinoma (NPC) 5-8F cell lines. Methods Western blotting was used to detect the protein levels of FOXC1 in human immortalized nasopharyngeal cell lines NP69, nasopharyngeal carcinoma cell lines 6-10B with lower metastasis potential and nasopharyngeal carcinoma cell lines 5-8F with higher metastasis potential. siRNA was used to downregulate the expression of FOXC1 in 5-8F cell lines, and then ability of migration and invasion were observed. Results FOXC1 protein expression level in NP69 cell lines, 6-10B cell lines and 5-8F cell lines were (0.27 ± 0.04), (0.7 ± 20.06), (1.08 ± 0.05) respectively, and the difference was statistically significant (P < 0.05). Also ability of cell migration and invasion significantly weakened after FOXC1 depletion in 5-8F cell lines (P < 0.05). Conclusion FOXC1 might regulate invasion and metastasis of nasopharyngeal carcinoma through changing expression of Fibronectin and Vimentin, and FOXC1 may be an available target for molecular target therapy of nasopharyngeal carcinoma.
2.Expression of FOXC1 and its relationship with E-cadherin in nasopharyngeal carcinoma tissues.
Peng LIU ; Shengkui TAN ; Shengjun XIAO ; Shijiang YI ; Lei OUYANG ; Qiaoyan HOU ; Weiming XIONG ; Xun LEI
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2014;28(15):1109-1112
OBJECTIVE:
To investigate the significance and relationship between the expression of FOXC1 and clinicopathological features, and to explore its correlation with E-cadherin.
METHOD:
Immunohistochemical SP method was used to detected the expression of FOXC1 in nasopharyngeal carcinoma tissues and nasopharyngitis tissues.
RESULT:
(1) Immunoreaction to FOXC1 was mainly located in nucleus of nasopharyngeal carcinoma cells. The positive expression rate of FOXC1 in nasopharyngeal carcinoma tissues was 85.3% (81/95), which was significantly higher than that in nasopharyngitis tissues (59.4%) (P < 0.05). (2) The expression of FOXC1 was not related to patients' age and gender, clinical stage of cancer and lymph node metastasis (P > 0.05). (3) There was a correlation between the expression of FOXC1 and down-regulated expression of E-cadherin in nasopharyngeal carcinoma tissues (P < 0.05).
CONCLUSION
FOXC1 may play an important role in generation and progression of nasopharyngeal carcinoma, there may be a correlation between the expression of FOXC1 and down-regulated expression of E-cadherin, also FOXC1 may play an important role in the process of EMT in nasopharyngeal carcinoma by regulating E-cadherin.
Adolescent
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Adult
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Aged
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Antigens, CD
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Cadherins
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metabolism
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Carcinoma
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Female
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Forkhead Transcription Factors
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metabolism
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Humans
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Male
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Middle Aged
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Nasopharyngeal Carcinoma
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Nasopharyngeal Neoplasms
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metabolism
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pathology
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Nasopharyngitis
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metabolism
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Young Adult
3.Signifinace of cyclin D1 expression in CNE2 cells processed by EGCG.
Zifang LI ; Wenhua WANG ; Xiaosong HE ; Guangxu XUAN ; Shijiang YI ; Wei ZHANG ; Lanzhen HUANG
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2014;28(9):585-592
OBJECTIVE:
To study the expression of Cyclin D1 in nasopharyngeal carcinoma cells processed by epigallocatechin gallate(EGCG) and it's significance, and revealed the anti-tumor mechanism of EGCG against nasopharyngeal carcinoma.
METHOD:
CNE-2 cells were treated by EGCG at different concentrations, the morphological changes of CNE-2 cells were observed by inverted microscope; the inhibition ratio of cell proliferation was detected by MTT colorimetric method, flow cytometry was used to analyze the changes of cell cycle. The expression of Cyclin D1 mRNA was detected by RT-PCR.
RESULT:
After treated by EGCG, the CNE2 cells decreased in amount and density, some of which became roll and small; Floating and dead cells can be seen in the inverted microscopy; cell proliferation was significantly inhibited in a time and dose dependent (P < 0.05). CNE-2 cells were arrested at G1/G0 phase. The expression of Cyclin D1 mRNA was down-regulated by EGCG with concentration and action time dependent (P < 0.05).
CONCLUSION
EGCG resisted nasopharyngeal carcinoma by inhibiting the cell proliferation, The down regulation of Cyclin D1 mRNA expression in a time and dose dependent may be the possible mechanisms.
Carcinoma
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Catechin
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analogs & derivatives
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pharmacology
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Cell Cycle
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drug effects
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Cell Line, Tumor
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Cell Proliferation
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drug effects
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Cyclin D1
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metabolism
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Humans
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Nasopharyngeal Carcinoma
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Nasopharyngeal Neoplasms
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metabolism
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pathology
4.Effects of EGCG on the nasopharyngeal carcinoma cell line CNE-2 and the expression of related gene.
Xun LEI ; Zhongyu KONG ; Caiwen FAN ; Shijiang YI ; Qiu XIANG ; Qianghe LIU
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2012;26(15):697-700
OBJECTIVE:
To study the effects of epigallocatechin-3-gallate (EGCG) on proliferation and apoptosis of nasopharyngeal carcinoma CNE-2 cell line and analyze the expression of Bcl-2, Bax and Caspase-3 in the cell line which treated with EGCG.
METHOD:
MTT assay and flow cytometry were used to analyze cell proliferation and cell cycle. Hoechst33258 fluorescence staining was adopted to study cell apoptosis. RT-PCR was used to detect the expression of Bcl-2, Bax, Caspase-3.
RESULT:
EGCG could significantly inhibit proliferation of CNE-2 cell line and induce its apoptosis with dose-independent relationship. EGCG could suppress the expression of Bcl-2 and induce expression of Bax, Caspase-3.
CONCLUSION
EGCG in vitro has efficacy of anti-nasopharyngeal carcinoma cells, which may be through regulating the expression of cell proliferation and apoptosis genes involved.
Apoptosis
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drug effects
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Carcinoma
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Caspase 3
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metabolism
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Catechin
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analogs & derivatives
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pharmacology
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Cell Line, Tumor
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Cell Proliferation
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drug effects
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Humans
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Nasopharyngeal Carcinoma
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Nasopharyngeal Neoplasms
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metabolism
;
pathology
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Proto-Oncogene Proteins c-bcl-2
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metabolism
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bcl-2-Associated X Protein
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metabolism