|Table of Contents|

Expression of TRIM29 in gliomas and its effect on proliferation and migration of glioblastoma U-87 MG cells

(PDF)

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

Issue:
2018年第11期
Page:
959-965
Research Field:
基础医学
Publishing date:

Info

Title:

Expression of TRIM29 in gliomas and its effect on proliferation and migration of glioblastoma U-87 MG cells

Author(s):

WANG Yutao ZHOU Ji YANG Dong ZHANG Yundong

Department of Neurosurgery, Institute of Surgery Research, Third Affiliated Hospital, Army Medical University (Third Military Medical University), Chongqing, 400042; Department of Neurosurgery, General Hospital of PLA Rocket Force, Beijing, 100088; 3Department of Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, 401120, China

Keywords:

TRIM29 glioblastoma proliferation migration

PACS:
R394.2; R730.23; R730.264
DOI:
-
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 (r=0.535, P<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 (P<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, P<0.05) and that of shScramble group (1.51±0.05, P<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 (P<0.05). In addition, the knockdown of TRIM29 also decreased the p-AKT protein level (P<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.

References:

[1]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.
[2]MEYER M A. Malignant gliomas in adults[J]. N Engl J Med, 2008, 359(17): 1850; author reply 1850. DOI:10.1056/NEJMc086380.
[3]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.
[4]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.
[5]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.
[6]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.
[7]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.
[8]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.
[9]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.
[10]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.
[11]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.
[12]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.
[13]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.
[14]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.
[15]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.
[16]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.

Memo

Memo:
-
Last Update: 2018-06-13