期刊文献+

hsa-miR-34b-3p与CDK4在骨肉瘤组织中的表达水平及临床意义 被引量:1

Expressions of hsa-miR-34b-3p and CDK4 in Osteosarcoma and Their Clinical Significance
下载PDF
导出
摘要 目的探究hsa-miR-34b-3p(miR-34b)与CDK4在骨肉瘤中表达水平,并分析临床意义。方法选取100例冻存骨肉瘤组织及其对应的癌旁组织标本。使用qRT-PCR检测组织中miR-34b表达水平。使用WB检测CDK4蛋白的表达水平。结果与癌旁非肿瘤组织相比,骨肉瘤组织中miR-34b表达水平显著降低,而CDK4蛋白的表达显著增高,差异具有统计学意义(P<0.05)。在骨肉瘤组织中,miR-34b的表达随肿瘤分期进展而逐渐降低,而CDK4蛋白的表达逐渐增高,miR-34b表达与CDK4蛋白表达呈负相关。在软组织浸润和转移者中miR-34b的表达水平显著低于软组织无浸润和无转移者,而CDK4蛋白表达则相反。结论在骨肉瘤组织中,miR-34b的表达随临床分期进展而逐渐降低,可能通过负向调控CDK4表达而在骨肉瘤发生发展过程中发挥作用。 Objective To investigate the expression of hsa-miR-34b-3p(miR-34b) and CDK4 in osteosarcoma,and analyze the clinical significance. Methods 100 cases of cryosurgery osteosarcoma tissues and their corresponding adjacent tissue specimens were selected.qRT-PCR was used to detect miR-34b expression in the tissues.WB was used to detect the expression level of CDK4 protein. Results Compared with adjacent tissue,the expression of miR-34b in osteosarcoma tissue significantly reduced while the expression of CDK4 protein significantly increased( P 〈0.05).In osteosarcoma tissues,the expression of miR-34b gradually decreased as the stage of tumor progressed,while the expression of CDK4 protein gradually increased,and the expression of miR-34b was negatively correlated with CDK4 protein.The expression of miR-34b in soft tissue infiltrating and metastatic patients was significantly lower than those in soft tissue without invasion and metastasis.However,CDK4 protein expression was the opposite. Conclusion In osteosarcoma tissues,the expression of miR-34b decreases gradually with the progression of clinical stage,and may play a role in the development of osteosarcoma by negatively regulating the expression of CDK4.
作者 宋光泽 赵慧霞 SONG Guangze;ZHAO Huixia(First Affiliated Hospital of PLA General Hospital,Beijing,100048)
出处 《实用癌症杂志》 2018年第7期1093-1096,共4页 The Practical Journal of Cancer
关键词 骨肉瘤 hsa-miR-34b-3 CDK4 临床意义 Osteosarcoma Hsa-miR-34b-3p CDK4 Clinical significance
  • 相关文献

参考文献2

二级参考文献21

  • 1Veremeyko T, Siddiqui S, Sotnikov I, Yung A and Ponomarev ED. IL-4/ IL-13-dependent and independent expression of miR-124 and its contribu- tion to M2 phenotype of monocytic cells in normal conditions and during allergic inflammation. PLoS One 2013, 8:e81774.
  • 2Li D, Lu Z, Jia J, Zheng Z and Lin S. MiR-124 is related to podocytic adhe- sive capacity damage in STZ-induced uninephrectomized diabetic rats. Kidney Blood Press Res 2013, 37: 422-431.
  • 3Lu Y, Yue X, Cui Y, Zhang J and Wang K. MicroRNA-124 suppresses growth of human hepatoeellular carcinoma by targeting STAT3. Biochem Biophys Res Commun 2013, 441: 873- 879.
  • 4Laine SK, Aim JJ, Virtanen SP, Aro HT and Laitala-Leinonen TK. MicroRNAs miR-96, miR-124, and miR-199a regulate gene expression in human bone marrow-derived mesenchymal stem cells. J Cell Biochem 2012, 113: 2687-2695.
  • 5Li KK, Pang JC, Ching AK, Wong CK, Kong X, Wang Y and Zhou L, et al. miR-124 is frequently down-regulated in medulloblastoma and is a negative regulator ofSLC 16A1. Hum Patho12009, 40: 1234-1243.
  • 6Liang YJ, Wang QY, Zhou CX, Yin QQ, He M, Yu XT and Cao DX, et al. MiR-124 targets slug to regulate epithelial-mesenchymal transition and metastasis of breast cancer. Carcinogenesis 2013, 34: 713-722.
  • 7Liu X, Li F, Zhao S, Luo Y, Kang J, Zhao H and Yan F, et al. MicroRNA-124-mediated regulation of inhibitory member of apoptosis- stimulating protein of p53 family in experimental stroke. Stroke 2013, 44: 1973- 1980.
  • 8Makeyev EV, Zhang J, Carrasco MA and Maniatis T. The microRNA miR-124 promotes neuronal differentiation by triggering brain-specific al- ternative pre-mRNA splicing. Mol Cell 2007, 27: 435-448.
  • 9Shi XB, Xue L, Ma AH, Tepper CG, Gandour-Edwards R, Kung HJ and deVere White RW. Tumor suppressive miR-124 targets androgen receptor and inhibits proliferation of prostate cancer cells. Oncogene 2013, 32: 4130-4138.
  • 10Sonntag KC, Woo TU and Krichevsky AM. Converging miRNA functions in diverse brain disorders: a case for miR-124 and miR-126. Exp Neurol 2012, 235: 427-435.

共引文献16

同被引文献14

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部