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骨肉瘤病灶内叉头框转录因子M1基因表达与癌基因表达的相关性 被引量:2

Correlation between the expression of FoxM1 gene and the expression of oncogene in osteosarcoma lesions
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摘要 目的探讨骨肉瘤病灶内叉头框转录因子M1(Fox M1)基因表达与癌基因表达的相关性。方法选取2013年1月至2017年12月间汉中市中心医院收治的行手术切除的80例骨肉瘤患者作为骨肉瘤组,选取同期行手术治疗的50例骨折患者作为对照组。收集患者的骨肉瘤病灶及正常碎骨组织,测定并比较Fox M1基因及癌基因的表达量。结果骨肉瘤组患者病灶内Fox M1、Livin、Cyclin D、Notch3、FAK和N-cadherin基因的mRNA表达量明显高于对照组患者,而TAp73、Beclin1、PTEN、Caspase-8和E-cadherin的mRNA表达量明显低于对照组患者,差异均有统计学意义(均P <0. 05)。Fox M1基因的mRNA表达量与TAp73、Beclin1、PTEN、Caspase-8和E-cadherin的mRNA表达量呈负相关,Fox M1基因的mRNA表达量与Livin、Cyclin D、Notch3、FAK和N-cadherin的mRNA表达量呈正相关,差异均有统计学意义(均P <0. 05)。结论骨肉瘤病灶内Fox M1基因的高表达能够促进原癌基因表达,减少抑癌基因表达。 Objective To study the correlation between the expression of Forkhead box M1( Fox M1) gene and the expression of oncogene in osteosarcoma. Methods Eighty patients with osteosarcoma who received surgery at Hanzhong Center Hospital from January 2013 to December 2017 were selected as the osteosarcoma group,and 50 fracture patients who received surgery at the hospital during the same time were selected as the control group. Then osteosarcoma lesions and normal bone fragments were collected,and the expression of Fox M1 gene and oncogene were measured. Results The mRNA expression of Fox M1,Livin,Cyclin D,Notch 3,FAK and N-cadherin gene was significantly higher in osteosarcoma group than in the control group,and the mRNA expression of TAp73,Beclin1,PTEN,Caspase-8 and E-cadherin was significantly lower in osteosarcoma group than in the control group. The mRNA expression level of Fox M1 was negatively correlated with the mRNA expression of TAp73,Beclin1,PTEN,Caspase-8 and E-cadherin,but positively correlated with the mRNA expression of Livin,Cyclin D,Notch 3,FAK and N-cadherin( all P < 0. 05). Conclusion The high expression of Fox M1 gene in osteosarcoma can promote the expression of oncogene and reduce the expression of tumor suppressor gene.
作者 强廷会 周新立 郭忠尚 牟欢 杜兴国 高飞 杨旻 QIANG Ting-hui;ZHOU Xin-li;GUO Zhong-shang;MOU Huan;DU Xing-guo;GAO Fei;YANG Min(Department of Orthopedic Surgery,Hanzhong Center Hospital,Hanzhong 723100,China;Department of Orthopedics,Military Medical University Affiliated Xijing Hospital,Xi'an 710032,China)
出处 《中国肿瘤临床与康复》 2018年第12期1431-1434,共4页 Chinese Journal of Clinical Oncology and Rehabilitation
基金 国家自然科学基金资助项目(61102029)
关键词 骨肉瘤 叉头框转录因子M1 原癌基因 抑癌基因 Osteosarcoma Forkhead box M1 Proto-oncogene Tumor suppressor gene
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  • 1杨彤涛,张志培,李存孝,高杰,张勇,周勇,范清宇,马保安.RNA干涉技术抑制骨肉瘤细胞MG63中Survivin基因表达的研究[J].中华肿瘤防治杂志,2007,14(10):744-748. 被引量:3
  • 2Schwab JH, Springfield DS, Raskin KA, et al. What's new in primary bone tumors[J]. J Bone Joint Surg Am,2012,94(20): 1913-1919.
  • 3Korver W, Roose J. The winged-helix transcription factor Tri- dent is expressed in cycling cells[J]. Nucleic Acids Res, 1997, 25(9) :1715-1719.
  • 4Yao KM, Sha M, Lu Z, et al. Molecular analysis of a novel winged helix protein, WIN. Expression pattern, DNA binding property, and alternative splicing within the DNA binding do- main[J]. J BioI Chem, 1997,272(32) :1927-1936.
  • 5Wierstra I, Alves J. FoxM1 a typical proliferation-associated transcription factor[J]. Biol Chem, 2007,388 (12) : 1257-1274.
  • 6Gialmanidis IP,Bravou V, Amanetopoulou SG, et al. Overexpres-sion of hedgehog pathway molecules and FOXM1 in non-small cell lung carcinomas[J]. Lung Cancer, 2009,66 (1) : 64-74.
  • 7Yang C, Chen H, Tan G, et al. FOXM1 promotes the epithelial to mesenchymal transition by stimulating the transcription of Slug in human breast cancerFJ]. Cancer letters, 2013, 340(1) : 104-112.
  • 8Cai Y, Balli D, Ustiyan V, et al. Foxml expression in prostate epithelial cells is essential for prostate carcinogenesis[J]. J Biol Chem, 2013, 288(31): 22527-22541.
  • 9Wierstra I, Alves .l. FoxMlc is activated by cyclin E/Cdk2, cyc- lin A/Cdk2, and cyclin A/Cdkl, but repressed by GSK-Salpha [J]. Biochem Biophys Res Commun, 2006,348 ( 1 ) : 99-108.
  • 10Wang IC, Chen YJ. FoxM1 regulates transcription of JNK1 to promote the G1/S transition and tumor cell invasiveness[J]. J Biol Chem,2008,283(30) : 20770-20778.

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