TRIM59 overexpression correlates with poor prognosis and contributes to breast cancer progression through AKT signaling pathway

Liu, Yunxiao; Dong, Yanyan; Zhao, Liping; Su, Lihong; Diao, Kexin; Mi, Xiaoyi

doi:10.1002/mc.22897

Cited by 40 publications

(30 citation statements)

References 23 publications

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“…Furthermore, overexpression of TRIM44 enhanced the migratory and invasive abilities of the lung cancer cell lines A549 and H441 (34). Previous studies reported that TRIM59 was associated with the genesis, development and prognosis of tumors (12,15,35). For example, TRIM59 was upregulated and promoted cell proliferation, migration and invasion in human osteosarcoma (36).…”

Section: Discussionmentioning

confidence: 87%

“…A previous study revealed that upregulated TRIM59 served as a proto-oncogene and induced the progression of prostate cancer in transgenic mice (38). The upregulation of TRIM59 not only enhanced the expression of cyclin A, cyclin E, Bcl-xl, Bcl-2 and phosphorylated-AKT, and downregulated the expression of p21, p27 and p53, resulting in poor prognosis in breast cancer, but also affect breast cancer progression via the AKT signaling pathway (12). The aforementioned studies suggested that TRIM59 regulates a diverse range of cellular functions during tumor progression.…”

Section: Discussionmentioning

confidence: 98%

“…Due to the highly conserved RING domain, the majority of the proteins are E3 ubiquitin ligases that promote post-translational modifications of various substrates (10) and affect a range of cellular processes, including cell growth, development, differentiation, apoptosis, inflammation and immunity (11). TRIM59 not only participates in regulating protein expression, but also in the malignant behavior of tumor cells (12).…”

Section: Introductionmentioning

confidence: 99%

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TRIM59 as a novel molecular biomarker to predict the prognosis of patients with NSCLC

et al. 2019

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As a member of the tripartite motif family, tripartite motif-containing protein 59 (TRIM59) serves as an E3 ubiquitin ligase in various cellular processes, including intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. The present study aimed to investigate the expression and prognostic value of TRIM59 in patients with non-small cell lung cancer (NSCLC). Expression of TRIM59 in patients with NSCLC was measured by immunohistochemistry in tissue microarrays. Datasets from The Cancer Genome Atlas (TCGA) were used to further verify the expression level of TRIM59 in NSCLC, lung adenocarcinoma and lung squamous cell carcinoma (LUSC). The prognostic value of TRIM59 in NSCLC was also analyzed. Immunohistochemistry revealed that TRIM59 was primarily located in the cytoplasm of tumor cells. Analysis of TCGA datasets revealed that TRIM59 was more highly expressed in tumor tissues than in normal tissues (P<0.0001). Furthermore, the TRIM59 expression level was associated with tumor differentiation (P=0.012), while no association was observed between TRIM59 expression and any other clinicopathological parameters. However, the average overall survival rate of patients with NSCLC in the high TRIM59 expression group was significantly lower than that in the low expression group (P=0.014), especially in patients with LUSC (P=0.016) and patients with poor differentiation (P=0.033). The multivariate analysis indicated that high TRIM59 expression is an independent prognostic factor in patients with NSCLC (P=0.018) and was associated with poor prognosis in patients with NSCLC. Therefore, TRIM59 may serve as a novel molecular biomarker to predict the prognosis of patients with NSCLC.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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TRIM59 as a novel molecular biomarker to predict the prognosis of patients with NSCLC

et al. 2019

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“…Current research focused on the function of TRIM59 in various types of cancer and has demonstrated that TRIM59 can regulate the PI3K/AKT signal pathway in various cancers. TRIM59 promotes neuroblastoma through the Wnt/beta-catenin (24) and PI3K/AKT signaling pathways (18), accelerates bladder cancer via the TGF-beta/Smad2/3 signaling pathway (25), and facilitates breast cancer (26), cholangiocarcinoma (17,19), and ovarian cancer (27) through the PI3K/AKT signaling pathway. PI3K/AKT is also related to inflammation by activating IKKα and the whole NF-κB signal pathway (20).…”

Section: Discussionmentioning

confidence: 99%

TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages

et al. 2020

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Sepsis is associated with bacterial invasion and inflammation and has a high mortality rate. Previous studies have demonstrated that tripartite motif 59 (TRIM59) was involved in NF-κB signaling and could promote phagocytosis of macrophages, but the role of TRIM59 in sepsis is still unknown. In our study, we found that TRIM59 was downregulated in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs). In the cecal ligation and puncture (CLP) sepsis mice model, the mortality of Trim59 flox/flox Lyz-Cre (Trim59-cKO) mice was higher, the immune cell infiltration and damage of liver and lung were more severe, and bacteria burden was increased. We also found that TRIM59 altered the production of pro-inflammation cytokines, as well as macrophage phagocytosis ability. Further analysis indicated that NF-κB signal pathway and Fcγ receptors might be involved in these regulations. Our study demonstrated for the first time that TRIM59 protects mice from sepsis by regulating inflammation and phagocytosis in macrophages.

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“… 28 , 29 Elevated TRIM59 expression is correlated with a relatively poor prognosis and progression in breast cancer. 30 Knocking down TRIM59 expression remarkably inhibits cell proliferation in neuroblastoma, 31 hepatocellular carcinoma, 32 and cholangiocarcinoma. 33 However, to date, the role of TRIM59 in retinoblastoma has not been reported.…”

Section: Discussionmentioning

confidence: 99%

TRIM59 Promotes Retinoblastoma Progression by Activating the p38–MAPK Signaling Pathway

Shang

You

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Retinoblastoma is a malignant tumor of the developing retina that mostly occurs in children. Our study aimed to investigate the effect of tripartite motif-containing protein 59 (TRIM59) on retinoblastoma growth and the underlying mechanisms. METHODS. We performed bioinformatic analysis of three datasets (GSE24673, GSE97508, and GSE110811) from the Gene Expression Omnibus database. Quantitative reversetranscription PCR and immunoblotting of three retinoblastoma cell lines were conducted to verify TRIM59 as a differentially expressed gene. Specific siRNAs were used to inhibit TRIM59 expression in the HXO-Rb44 cell line. A lentiviral vector was transfected into the Y79 cell line to overexpress TRIM59. The effects of TRIM59 on retinoblastoma cell proliferation, cell cycling, and apoptosis were explored in vitro using the abovementioned cell lines. The effect of TRIM59 expression on retinoblastoma cell proliferation was evaluated in a mouse xenograft tumor model. RESULTS. TRIM59 expression in three retinoblastoma cell lines was remarkably elevated compared with normal control. Knocking down TRIM59 expression remarkably suppressed cell proliferation and growth and promoted cell apoptosis in HXO-Rb44 cells, whereas TRIM59 overexpression promoted tumor progression in Y79 cells. Silencing TRIM59 also markedly inhibited in vivo tumor growth in the xenograft model. Mechanistic studies revealed that TRIM59 upregulated phosphorylated p38, p-JNK1/2, p-ERK1/2, and p-c-JUN expression in retinoblastoma cells. Notably, the p38 inhibitor SB203580 attenuated the effects of TRIM59 on cell proliferation, apoptosis, and the G 1 /S phase transition. CONCLUSIONS. TRIM59 plays an oncogenic role in retinoblastoma and exerts its tumorpromotive function by activating the p38-mitogen-activated protein kinase pathway.

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TRIM59 overexpression correlates with poor prognosis and contributes to breast cancer progression through AKT signaling pathway

Cited by 40 publications

References 23 publications

TRIM59 as a novel molecular biomarker to predict the prognosis of patients with NSCLC

TRIM59 as a novel molecular biomarker to predict the prognosis of patients with NSCLC

TRIM59 Protects Mice From Sepsis by Regulating Inflammation and Phagocytosis in Macrophages

TRIM59 Promotes Retinoblastoma Progression by Activating the p38–MAPK Signaling Pathway

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