TRIM29基因在胶质瘤中的表达及其对胶质母细胞瘤细胞U-87 MG增殖与迁移的影响

王雨涛; 周济; 杨冬; 张云东

doi:10.16016/j.1000-5404.201802062

您当前的位置：

首页 >

文章列表页 >

TRIM29基因在胶质瘤中的表达及其对胶质母细胞瘤细胞U-87 MG增殖与迁移的影响

基础医学 | 更新时间：2026-01-09

- TRIM29基因在胶质瘤中的表达及其对胶质母细胞瘤细胞U-87 MG增殖与迁移的影响
- Expression of TRIM29 in gliomas and its effect on proliferation and migration of glioblastoma U-87 MG cells
- 第三军医大学学报 2018年40卷第11期页码：959-965
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.16016/j.1000-5404.201802062
  中图分类号：
- 收稿：2018-02-08，
  
  纸质出版：2018-06
- 稿件说明：
移动端阅览
王雨涛, 周济, 杨冬, 等. TRIM29基因在胶质瘤中的表达及其对胶质母细胞瘤细胞U-87 MG增殖与迁移的影响[J]. 第三军医大学学报, 2018,40(11):959-965.

Yutao WANG, Ji ZHOU, Dong YANG, et al. Expression of TRIM29 in gliomas and its effect on proliferation and migration of glioblastoma U-87 MG cells[J]. Journal of Third Military Medical University, 2018, 40(11): 959-965.
王雨涛, 周济, 杨冬, 等. TRIM29基因在胶质瘤中的表达及其对胶质母细胞瘤细胞U-87 MG增殖与迁移的影响[J]. 第三军医大学学报, 2018,40(11):959-965. DOI： 10.16016/j.1000-5404.201802062.

Yutao WANG, Ji ZHOU, Dong YANG, et al. Expression of TRIM29 in gliomas and its effect on proliferation and migration of glioblastoma U-87 MG cells[J]. Journal of Third Military Medical University, 2018, 40(11): 959-965. DOI： 10.16016/j.1000-5404.201802062.

摘要

Abstract

Objective

To observe the expression of TRIM29 in glioma tissues and its relationship with clinicopathological features

and to determine its effect on the proliferation and migration of glioblastoma U-87 MG cells and investigate its possible mechanism.

Methods

Immunohistochemical assay was used to detect the expression of TRIM29 protein in 56 samples of glioma tissues and normal brain tissues

and the relationship between TRIM29 protein level and clinicopathological features was analyzed. Western blotting was used to detect the expression of TRIM29 protein in the glioblastoma tissues

paracancerous tissues and normal tissues

and in different glioma cell lines (A172

LN-229

U-87 MG and U-118 MG). RNA interference technique was used to treat the U-87 MG cells (with high expression of TRIM29)

and then the cells were divided into 3 groups: blank control group

shScramble group and shTRIM29 group. Subsequently

MTT assay

colony formation assay and Transwell chamber test were used respectively for the effects of TRIM29 knockdown on the proliferation and migration of the U-87 MG cells. The effect was further studied through nude mouse tumorigenesis assay. Finally

Western blotting was used to detect the changes of AKT pathway proteins after the knockdown of TRIM29.

Results

The expression of TRIM29 in glioma tissue was higher than that in normal brain tissue

and positively correlated with the WHO grade (

=0.535

0.05). Western blotting showed that the expression of TRIM29 protein was significantly up-regulated in glioblastoma tissues when compared with normal brain tissues and adjacent normal tissues (

0.05). The protein level of TRIM29 was 0.27±0.02

0.69±0.04

1.24±0.08 and 0.82±0.06

respectively in glioma A172

LN-229

U-87 MG and U-118 MG cells. In the U-87 MG cells after RNA interference

the protein expression of TRIM29 was 0.27±0.04

significantly lower than that of the blank control group (1.64±0.05

0.05) and that of shScramble group (1.51±0.05

0.05). The proliferation and migration were significantly decreased of in the TRIM29 knockdown U-87 MG cells than the blank control and negative control groups (

0.05). In addition

the knockdown of TRIM29 also decreased the p-AKT protein level (

0.05).

Conclusion

TRIM29 is highly expressed in gliomas and positively correlated with tumor malignancy

and it may promote the proliferation and migration of the cells through the AKT signaling pathway.

关键词

Keywords

references

RIDDICK G FINE H A Integration and analysis of genome-scale data from gliomas Nat Rev Neurol 2011 7 8 439 450 10.1038/nrneurol.2011.100 RIDDICK G, FINE H A. Integration and analysis of genome-scale data from gliomas[J]. Nat Rev Neurol, 2011, 7(8): 439-450. DOI:10.1038/nrneurol.2011.100.

MEYER M A Malignant gliomas in adults N Engl J Med 2008 359 17 1850 10.1056/NEJMc086380 MEYER M A. Malignant gliomas in adults[J]. N Engl J Med, 2008, 359(17): 1850; author reply 1850. DOI:10.1056/NEJMc086380.

KIM E KIM M WOO D H Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells Cancer Cell 2013 23 6 839 852 10.1016/j.ccr.2013.04.008 KIM E, KIM M, WOO D H, et al . Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells[J ] . Cancer Cell, 2013, 23(6): 839-852. DOI:10.1016/j.ccr.2013.04.008.

DAGOGO-JACK I SHAW A T Tumour heterogeneity and resistance to cancer therapies Nat Rev Clin Oncol 2018 15 2 81 94 10.1038/nrclinonc.2017.166 DAGOGO-JACK I, SHAW A T. Tumour heterogeneity and resistance to cancer therapies[J]. Nat Rev Clin Oncol, 2018, 15(2): 81-94. DOI:10.1038/nrclinonc.2017.166.

KIMURA T JIA J KUMAR S Dedicated SNAREs and specialized TRIM cargo receptors mediate secretory autophagy EMBO J 2017 36 1 42 60 10.15252/embj.201695081 KIMURA T, JIA J, KUMAR S, et al . Dedicated SNAREs and specialized TRIM cargo receptors mediate secretory autophagy[J ] . EMBO J , 2017, 36(1): 42-60. DOI:10.15252/embj.201695081.

SATO T TAKAHASHI H HATAKEYAMA S The TRIM-FLMN protein TRIM45 directly interacts with RACK1 and negatively regulates PKC-mediated signaling pathway Oncogene 2015 34 10 1280 1291 10.1038/onc.2014.68 SATO T, TAKAHASHI H, HATAKEYAMA S, et al . The TRIM-FLMN protein TRIM45 directly interacts with RACK1 and negatively regulates PKC-mediated signaling pathway[J ] . Oncogene, 2015, 34(10): 1280-1291. DOI:10.1038/onc.2014.68.

UCHIL P D HINZ A SIEGEL S TRIM protein-mediated regulation of inflammatory and innate immune signaling and its association with antiretroviral activity J Virol 2013 87 1 257 272 10.1128/JVI.01804-12 UCHIL P D, HINZ A, SIEGEL S, et al . TRIM protein-mediated regulation of inflammatory and innate immune signaling and its association with antiretroviral activity[J ] . J Virol, 2013, 87(1): 257-272. DOI:10. 1128/JVI.01804-12.

LOEDIGE I GAIDATZIS D SACK R The mammalian TRIM-NHL protein TRIM71/LIN-41 is a repressor of mRNA function Nucleic Acids Res 2013 41 1 518 532 10.1093/nar/gks1032 LOEDIGE I, GAIDATZIS D, SACK R, et al . The mammalian TRIM-NHL protein TRIM71/LIN-41 is a repressor of mRNA function[J ] . Nucleic Acids Res, 2013, 41(1): 518-532. DOI:10.1093/nar/gks1032.

MANDELL M A KIMURA T JAIN A TRIM proteins regulate autophagy:TRIM5 is a selective autophagy receptor mediating HIV-1 restriction Autophagy 2014 10 12 2387 2388 10.4161/15548627.2014.984278 MANDELL M A, KIMURA T, JAIN A, et al . TRIM proteins regulate autophagy: TRIM5 is a selective autophagy receptor mediating HIV-1 restriction[J ] . Autophagy, 2014, 10(12): 2387-2388. DOI:10.4161/15548627.2014.984278.

KOSAKA Y INOUE H OHMACHI T Tripartite motif-containing 29 (TRIM29) is a novel marker for lymph node metastasis in gastric cancer Ann Surg Oncol 2007 14 9 2543 2549 10.1245/s10434-007-9461-1 KOSAKA Y, INOUE H, OHMACHI T, et al . Tripartite motif-containing 29 (TRIM29) is a novel marker for lymph node metastasis in gastric cancer[J ] . Ann Surg Oncol, 2007, 14(9): 2543-2549. DOI:10.1245/s10434-007-9461-1.

KANNO Y WATANABE M KIMURA T TRIM29 as a novel prostate basal cell marker for diagnosis of prostate cancer Acta Histochem 2014 116 5 708 712 10.1016/j.acthis.2013.12.009 KANNO Y, WATANABE M, KIMURA T, et al . TRIM29 as a novel prostate basal cell marker for diagnosis of prostate cancer[J ] . Acta Histochem, 2014, 116(5): 708-712. DOI:10.1016/j.acthis.2013.12.009.

JIANG T TANG H M LU S Up-regulation of tripartite motif-containing 29 promotes cancer cell proliferation and predicts poor survival in colorectal cancer Med Oncol 2013 30 4 715 10.1007/s12032-013-0715-4 JIANG T, TANG H M, LU S, et al . Up-regulation of tripartite motif-containing 29 promotes cancer cell proliferation and predicts poor survival in colorectal cancer[J ] . Med Oncol, 2013, 30(4): 715. DOI:10.1007/s12032-013-0715-4.

TANG Z P DONG Q Z CUI Q Z Ataxia-telangiectasia group D complementing gene (ATDC) promotes lung cancer cell proliferation by activating NF-κB pathway PLoS ONE 2013 8 6 e63676 10.1371/journal.pone.0063676 TANG Z P, DONG Q Z, CUI Q Z, et al . Ataxia-telangiectasia group D complementing gene (ATDC) promotes lung cancer cell proliferation by activating NF-κB pathway[J ] . PLoS ONE, 2013, 8(6): e63676. DOI:10.1371/journal.pone.0063676.

LAI W ZHAO J ZHANG C Upregulated ataxia-telangiectasia group D complementing gene correlates with poor prognosis in patients with esophageal squamous cell carcinoma Dis Esophagus 2013 26 8 817 822 10.1111/j.1442-2050.2012.01400.x LAI W, ZHAO J, ZHANG C, et al . Upregulated ataxia-telangiectasia group D complementing gene correlates with poor prognosis in patients with esophageal squamous cell carcinoma[J ] . Dis Esophagus, 2013, 26(8): 817-822. DOI:10.1111/j.1442-2050.2012.01400.x.

AI L KIM W J ALPAY M TRIM29 suppresses TWIST1 and invasive breast cancer behavior Cancer Res 2014 74 17 4875 4887 10.1158/0008-5472.CAN-13-3579 AI L, KIM W J, ALPAY M, et al . TRIM29 suppresses TWIST1 and invasive breast cancer behavior[J ] . Cancer Res, 2014, 74(17):4875-4887. DOI:10.1158/0008-5472.CAN-13-3579.

STEGEMAN H SPAN P N KAANDERS J H Improving chemoradiation efficacy by PI3-K/AKT inhibition Cancer Treat Rev 2014 40 10 1182 1191 10.1016/j.ctrv.2014.09.005 STEGEMAN H, SPAN P N, KAANDERS J H, et al . Improving chemoradiation efficacy by PI3-K/AKT inhibition[J ] . Cancer Treat Rev, 2014, 40(10): 1182-1191. DOI:10.1016/j.ctrv.2014.09.005.

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

LAPTM4B在胶质瘤组织中表达及对细胞增殖和侵袭力的影响

β-arrestin1在口腔鳞状细胞癌中的表达及其对细胞增殖、迁移、侵袭的作用

CPNE3调控非小细胞肺癌细胞增殖、迁移、侵袭及其相关机制研究

RNA传感器IFIH1对HPV阳性的宫颈癌细胞增殖、迁移和侵袭的影响

1-磷酸鞘氨醇1型受体促进小鼠颈动脉损伤后血管内膜增生