التفاصيل البيبلوغرافية
| العنوان: |
Bit1 knockdown contributes to growth suppression as well as the decreases of migration and invasion abilities in esophageal squamous cell carcinoma via suppressing FAK-paxillin pathway |
| المؤلفون: |
Fan, Tianli, Chen, Jing, Zhang, Lirong, Gao, Pan, Hui, Yiran, Xu, Peirong, Zhang, Xiaqing, Liu, Hongtao |
| بيانات النشر: |
BioMed Central Ltd. |
| سنة النشر: |
2016 |
| المجموعة: |
BioMed Central |
| مصطلحات موضوعية: |
Bcl-2 inhibitor of transcription 1, FAK-paxillin pathway, esophageal squamous cell carcinoma, cell migration, cell invasion |
| الوصف: |
Background There is growing evidence that Bit1 exerts different roles in the development and progression of human cancers. Although Bit1 was highly exhibited in ESCC tissues in our previous study, its roles and molecular mechanisms implicated in development and progression of ESCC remain unknown. Methods Bit1 protein expression in ESCC cell lines and normal esophageal epithelial cell was detected by Western blotting. Bit1 protein expression mediated by Bit1 shRNA was investigated by Western blotting. MTT, migration assay, invasion experiment, ELISA and Flow cytometry were utilized to determine the effects of Bit1 knockdown on cell proliferation, migration, invasion and apoptosis, respectively. A xenograft model was used to examine in vivo tumourigenicity, and immunohistochemistry and TUNEL were utilized to evaluate the related protein expression and apoptosis. Gene microarray was determined by Agilent SurePrint G3 Human GE 8 × 60 K Microarray, the interaction of Bit1 and FAK proteins were detected by Immunoprecipitation and the key protein expressions of FAK-paxillin pathway were detected by Western blotting. Results We found Bit1 expression in all human ESCC cell lines tested was significantly higher than that in normal esophageal epithelial cell Het-1A ( P < 0.05), in which EC9706 presented the highest Bit1 level. Bit1 protein level was significantly downregulated at day 1 after transfection with specific shRNA against Bit1 ( P < 0.05). At days 2 and 3, Bit1 level reached the lowest value after transfection with Bit1 shRNA. Moreover, Bit1 depletion contributed to growth inhibition in vitro and in vivo , reduced cell migration and invasion abilities, and induced cell apoptosis in EC9706 and TE1 cells. More importantly, Bit1 downregulation significantly lowered Bcl-2 and MMP-2 levels in EC9706 xenografted tumor tissues, meanwhile triggered apoptosis after treatment with different doses of Bit1 shRNA. Further gene microarray revealed that 23 genes in Bit1-RNAi group were markedly downregulated, ... |
| نوع الوثيقة: |
report |
| اللغة: |
English |
| العلاقة: |
http://www.molecular-cancer.com/content/15/1/23Test |
| الإتاحة: |
http://www.molecular-cancer.com/content/15/1/23Test |
| حقوق: |
Copyright 2016 Fan et al. |
| رقم الانضمام: |
edsbas.5F745CB8 |
| قاعدة البيانات: |
BASE |
