Identification of a synonymous variant in TRIM59 gene for gastric cancer risk in a Chinese population

Luo, Dakui; Wang, Younan; Huan, Xiangkun; Huang, Chih Chia; Yang, Chao; Hong, Fan; Xu, Zekuan; Yang, Li

doi:10.18632/oncotarget.14075

Cited by 7 publications

(8 citation statements)

References 31 publications

(32 reference statements)

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“…The present study indicates that TRIM59 promotes CRC progression, which is similar to previous studies in other cancer types such as NSCLC (10), gastric cancer (9,21), renal cell carcinoma (11) and osteosarcoma (22). Significantly shortened survival is seen in patients with high TRIM59 expression compared with those with low TRIM59 expression.…”

Section: Discussionsupporting

confidence: 89%

Knockdown of tripartite motif-59 inhibits the malignant processes in human colorectal cancer cells

Chen²,

et al. 2017

Oncology Reports

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The aim of the present study was to clarify the clinical implication and functional role of tripartite motif-59 (TRIM59) in colorectal carcinoma (CRC) and explore the underlying mechanism of aberrant high expression of TRIM59 in cancer. We validated that TRIM59 was upregulated in CRC samples, and also demonstrated that its upregulation was associated with advanced tumor stage of CRC patients; and its high expression indicated shorter overall survival and faster recurrence. Knockdown of TRIM59 significantly inhibited cell proliferation, migration and invasion. Cell cycle analysis showed that TRIM59-depleted cells accumulated in S-phase. In addition, the cell cycle regulators CDC25C, cyclin B1 and cyclin D1 were decreased by TRIM59 siRNA mediated knockdown. Furthermore, the depletion of TRIM59 promoted apoptosis in cell culture as indicated by the cleavage of caspase-3 and PARP when TRIM59 was depleted. These results suggested that TRIM59 is upregulated in human colorectal tumors compared with non-tumor tissues. The level of TRIM59 is correlated with malignant features of CRC and may serve as potential therapeutic and preventive strategies for CRC.

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Section: Discussionsupporting

confidence: 89%

Knockdown of tripartite motif-59 inhibits the malignant processes in human colorectal cancer cells

Chen²,

et al. 2017

Oncology Reports

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“…p53 plays a vital role in the regulation if cell cycle transition, checkpoint activation, and apoptotic machinery in tumor cells, which control expression of p21 and p27 . It has been reported that TRIM59, as an E3 ubiquitin ligases, was able to interacted with p53, increasing its ubiquitination and degradation in gastric cancer cells . In osteosarcoma, TRIM59 could downregulate p53 in both U2OS and MG63 cells .…”

Section: Discussionmentioning

confidence: 95%

“…[25][26][27] It has been reported that TRIM59, as an E3 ubiquitin ligases, was able to interacted with p53, increasing its ubiquitination and degradation in gastric cancer cells. 28 In osteosarcoma, TRIM59 could downregulate p53 in both U2OS and MG63 cells. 29 However, knocked down TRIM59 did not upregulate p53 protein expression in lung cancer cells, suggesting its effect may be cell context dependent.…”

Section: Trim59 Activates Akt Signaling and Promotes P53 Ubiquitinamentioning

confidence: 97%

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

Liu

Dong

Zhao

et al. 2018

Molecular Carcinogenesis

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TRIM59 has been recently implicated in the carcinogenesis of several cancers such as lung cancer, gastric cancer, and bladder cancer. However, its expression pattern and clinical significance has not been investigated in human breast cancer. In the present study, we examined TRIM59 protein expression in 95 cases of breast cancer tissues using immunohistochemistry. We found that TRIM59 was upregulated in 42 out of 95 cases and correlated with TNM stage (P = 0.0056), lymph node metastasis (P = 0.0088) and poor prognosis (P = 0.0092). Importantly, TRIM59 level was higher in triple-negative breast cancer (TNBC) (P = 0.0157). Expression of TRIM59 protein was also upregulated in breast cancer cell lines compared to normal MCF-10A cell line. TRIM59 plasmid and shRNA transfection was performed in MCF-7 and SK-BR-3 cells respectively. TRIM59 overexpression promoted cell proliferation, invasion, migration, cell cycle transition, and paclitaxel resistance, whereas TRIM59 depletion showed the opposite results. Further analysis showed that TRIM59 overexpression upregulated expression of cyclinA, cyclinE, Bcl-xl, Bcl-2, p-AKT, and downregulated expression of p21, p27, p53. AKT inhibitor treatment abolished the effect of TRIM59 on Bcl-2 expression. TRIM59 overexpression also upregulated the level of p53 ubiquitination. In conclusion, TRIM59 overexpression correlates with poor prognosis and promotes malignant behavior through regulation of AKT pathway in human breast cancer.

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“…The occurrence and development of GC are influenced by a series of complex factors involving host genetic susceptibility and multiple environmental factors [ 3 ]. In previous epidemiological studies, several genetic polymorphisms were identified to impact the risk of GC [ 4 – 7 ].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in lncRNA PTENP1 and the Risk of Gastric Cancer in a Chinese Population

Jiang

et al. 2017

Disease Markers

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Long noncoding RNA (lncRNA) phosphatase and tensin homolog pseudogene 1 (PTENP1) is significantly downregulated in gastric cancer (GC), playing critical roles in GC progression. However, the association between PTENP1 genetic variants and GC risk has not yet been reported. Using TaqMan technology, three lncRNA PTENP1 tag single nucleotide polymorphisms (tagSNPs) (rs7853346 C>G, rs865005 C>T, and rs10971638 G>A) were genotyped in 768 GC patients and 768 cancer-free controls in a Chinese population. We found that subjects with rs7853346 G allele had a remarkably decreased risk of GC, compared with those carrying C allele (P = 0.011 in an additive model, P = 0.033 after Bonferroni's correction). The further stratified analyses showed that the link between variant genotypes of rs7853346 and decreased GC risk was more obvious in older subjects (≥60 years), nonsmokers, nondrinkers, and subjects without family history of GC. We also found that relative PTENP1 mRNA expression levels were higher in rs7853346 CG/GG genotype carriers than those with common genotype in both GC and normal tissues (P < 0.05). Besides, bioinformatics analyses revealed that rs7853346 may change the local folding structure and alter the target microRNAs (miRNAs) of PTENP1. In conclusion, our results suggested that lncRNA PTENP1 polymorphism rs7853346 may predict GC susceptibility.

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Identification of a synonymous variant in TRIM59 gene for gastric cancer risk in a Chinese population

Cited by 7 publications

References 31 publications

Knockdown of tripartite motif-59 inhibits the malignant processes in human colorectal cancer cells

Knockdown of tripartite motif-59 inhibits the malignant processes in human colorectal cancer cells

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

Polymorphisms in lncRNA PTENP1 and the Risk of Gastric Cancer in a Chinese Population

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