|本期目录/Table of Contents|

[1]蔡 隽. FOXQ1稳定表达乳腺癌细胞系的建立及鉴定[J].天津医科大学学报,2015,21(04):292-295.
 CAI Jun.Establishment and identification of cell lines with stable expression of FOXQ1 in MDA-MB-231-luc[J].Journal of Tianjin Medical University,2015,21(04):292-295.
点击复制

 FOXQ1稳定表达乳腺癌细胞系的建立及鉴定(PDF)
分享到:

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
21
期数:
2015年04期
页码:
292-295
栏目:
基础医学
出版日期:
2015-07-15

文章信息/Info

Title:
Establishment and identification of cell lines with stable expression of FOXQ1 in MDA-MB-231-luc
文章编号:
1006-8147(2015)04-0292-04
作者:
蔡 隽
(天津医科大学肿瘤医院肿瘤研究所,国家肿瘤临床医学研究中心,天津市“肿瘤防治”重点实验室,乳腺癌防治教育部重点实验室,天津300060 )
Author(s):
CAI Jun
(1. Cancer Institute and Hospitai,Tianjin Medical University,National Clinical Research Center of Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy,  Key Laboratory of Breast Cancer Prevention and Therapy,Tianjin Medical University, Ministry of Education, Tianjin 300060, China)
关键词:

FOXQ1过表达乳腺癌迁移侵袭

Keywords:
FOXQ1 over-expression breast cancer migration invasion
分类号:
R737.9
DOI:
-
文献标志码:
A
摘要:

目的:建立稳定过表达FOXQ1乳腺癌细胞系,为进一步研究FOXQ1在体内乳腺癌转移、血管生成、抗凋亡机制,以及以FOXQ1为靶点开发抗肿瘤药物提供细胞研究模型。 方法:采用脂质体转染的方法将真核表达载体FOXQ1转染至MDA-MB-231-luc细胞,经G418筛选及克隆化培养,获得稳定过表达FOXQ1蛋白的细胞系。通过RT-PCR、Western blot和免疫荧光对细胞系中FOXQ1的表达和定位进行鉴定。通过Transwell迁移侵袭等实验,观察过表达FOXQ1后对231-luc细胞EMT相关蛋白表达、231-luc细胞迁移侵袭等生物学特性的影响。 结果:获得过表达FOXQ1的稳定细胞系,迁移侵袭实验表明该细胞系恶性化程度明显高于野生型。 结论:成功建立稳定过表达FOXQ1的乳腺癌细胞系,FOXQ1在细胞核中高表达,进而增加EMT间质标志物Fn1、Vim的表达,增强231-luc的迁移侵袭能力。

Abstract:
Objective: To investigate the contribution of temozolomide easter (TMZ-HE) to the proliferation and apoptosis of glioma LN-18 cells in vitro compared with temozolomide (TMZ). Methods: Methyl thiazolyl tetrazolium (MTT) assay was used to measure the effects on the proliferation of LN-18 cells cultured with graded concentrations of TMZ and TMZ-HE for 24, 48, 72 and 96 h. The long term effect was measured by colony formation assay. Hoechst 33342 and PI fluorescence staining were used to observe the cellular morphological changes and cell necrosis. The AnnexinV-fluoresce in isothiocyanate (FITC) and propidium iodide (PI) assay by flow cytometer were applied to detect the apoptosis induced by TMZ and TMZ-HE. Western blot detected the expressing of resistant protein MGMT in LN-18 after treatment with TMZ and TMZ-HE. Results: TMZ-HE obviously suppressed the proliferation of LN-18 cells in a concentration-and time-dependent manner compared with TMZ. TMZ-HE induced more cellular apoptosis of the LN-18 cells in a concentration-dependent manner. TMZ-HE could block the expressing of MGMT in LN-18 earlier than TMZ. Conclusion: TMZ-HE inhibits proliferation and induced apoptosis by blocked resistant protein MGMT in LN-18 cells. These effects are much stronger than TMZ.

参考文献/References:

[1] Hannenhalli S, Kaestner K H. The evolution of Fox genes and their role in development and disease [J]. Nat Rev Genet, 2009, 10(4): 233

[2] Wang W, He S, Ji J, et al. The prognostic significance of FOXQ1 oncogene overexpression in human hepatocellular carcinoma [J]. Pathol Res Pract, 2013, 209(6): 353

[3] Feng J, Zhang X, Zhu H, et al. FoxQ1 overexpression influences poor prognosis in non-small cell lung cancer, associates with the phenomenon of EMT [J]. PLoS One, 2012, 7(6): e39937

[4] Liang S H, Yan X Z, Wang B L, et al. Increased expression of FOXQ1 is a prognostic marker for patients with gastric cancer [J]. Tumour Biol, 2013, 34(5): 2605

[5] Kaneda H, Arao T, Tanaka K, et al. FOXQ1 is overexpressed in colorectal cancer and enhances tumorigenicity and tumor growth [J]. Cancer Res, 2010, 70(5): 2053

[6] Zhu Z, Pang Z, Xing Y, et al. Short hairpin RNA targeting FOXQ1 inhibits invasion and metastasis via the reversal of epithelial-mesenchymal transition in bladder cancer [J]. Int J Oncol, 2013, 42(4): 1271

[7] Zhang H, Meng F, Liu G, et al. Forkhead transcription factor foxq1 promotes epithelial-mesenchymal transition and breast cancer metastasis [J]. Cancer Res, 2011, 71(4): 1292

[8] Feuerborn A, Srivastava P K, Kuffer S, et al. The Forkhead factor FoxQ1 influences epithelial differentiation [J]. J Cell Physiol, 2011, 226(3): 710

[9] Micalizzi D S, Farabaugh S M, Ford H L. Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression [J]. J Mammary Gland Biol Neoplasia, 2010, 15(2): 117

[10] Xu J, Lamouille S, Derynck R. TGF-beta-induced epithelial to mesenchymal transition [J]. Cell Res, 2009, 19(2): 156

[11] Al Saleh S, Sharaf L H, Luqmani Y A. Signalling pathways involved in endocrine resistance in breast cancer and associations with epithelial to mesenchymal transition (Review) [J]. Int J Oncol, 2011, 38(5): 1197

[12] Philip R, Heiler S, Mu W, et al. Claudin-7 promotes the epithelial-mesenchymal transition in human colorectal cancer [J]. Oncotarget, 2015, 6(4):2046

[13] Tan E J, Kahata K, Idas O, et al. The high mobility group A2 protein epigenetically silences the Cdh1 gene during epithelial-to-mesenchymal transition [J]. Nucleic Acids Res, 2015, 43(1):162

[14] Jaspers J E, Sol W, Kersbergen A, et al. BRCA2-deficient sarcomatoid mammary tumors exhibit multi-drug resistance [J]. Cancer Res, 2015, 75(4):732

[15] Colombo F, Trombetta E, Cetrangolo P, et al. Giant lysosomes as a chemotherapy resistance mechanism in hepatocellular carcinoma cells [J]. PLoS One, 2014, 9(12): e114787

[16] Culjkovic-Kraljacic B, Zahreddine H A, Borden K L. Inducible drug modification: A new form of resistance [J]. Cell Cycle, 2014, 13(16): 2485

[17] Taube J H, Herschkowitz J I, Komurov K, et al. Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes [J]. Proc Natl Acad Sci U S A, 2010, 107(35): 15449



相似文献/References:

备注/Memo

备注/Memo:
作者简介 蔡隽(1989-),女,硕士在读,研究方向:生物化学与分子生物学;E-mail:caijun9865@126.com。
更新日期/Last Update: 2015-07-16