TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

Yang, Wei; Liu, Li; Li, Caixia; Luo, Ning; Chen, Rong; Li, Li; Yu, Fudong; Cheng, Zhongping

doi:10.1038/s41419-018-0881-6

Cited by 72 publications

(67 citation statements)

References 28 publications

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“…Tripartite motif (TRIM) proteins were the member of the RING family of E3 ubiquitin ligase, including RING-finger domain, Zinc-binding domain (B-boxes domain), Coiled-coil domain, and C-terminal domain, and the presence of RING finger indicated that TRIM protein as E3 participated in various physiological processes in cells [10][11][12][13]. Previous studies had reported the important functions of TRIM proteins in the development of various cancers, which played an important role in cell cycle, apoptosis, differentiation, metabolism, and immune response [14][15][16][17]. The clinical manifestations observed in human diseases caused by TRIM gene mutations might be due to change in TRIM activity during ubiquitination [18,19].…”

Section: Introductionmentioning

confidence: 99%

Tripartite motif containing 35 contributes to the proliferation, migration, and invasion of lung cancer cellsin vitroandin vivo

Zhang

et al. 2020

Bioscience Reports

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The tripartite motif (TRIM) family is a family of proteins with highly conserved domains. Previous researches have suggested that the members of TRIM family proteins played a crucial role in cancer development and progression. Our study explored the relationship between TRIM35 and non-small cell lung cancer (NSCLC). The study showed that the expression of TRIM35 was increased in NSCLC samples, and patients with high expression of TRIM35 had a poor clinical prognosis. Overexpression of TRIM35 in NSCLC cell line H460 promoted cell proliferation, migration, and invasion, knockdown of TRIM35 produced an opposite result in A549 and H1299 cell lines. In vivo study further confirmed that overexpression of TRIM35 promoted tumor formation. The RNA-seq analysis suggested that TRIM35 might promote lung cancer proliferation, migration, and invasion by regulating cancer-associated functions and signaling pathways. Hence, we identified TRIM35 played a significant role in tumoral growth and was a potential diagnosis and prognosis target for lung cancer.

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Section: Introductionmentioning

confidence: 99%

Tripartite motif containing 35 contributes to the proliferation, migration, and invasion of lung cancer cellsin vitroandin vivo

Zhang

et al. 2020

Bioscience Reports

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“…The tripartite motif23 may interact with these cytokines to positively regulate NF‐κB signaling. Recent studies have suggested that TRIM family proteins play a critical role in regulation of the NF‐κB pathway by ubiquitinating proteins at different steps . We performed GSEA analysis and found that high expression of TRIM23 was correlated with apoptosis resistance and DNA repair.…”

Section: Discussionmentioning

confidence: 93%

Elevated TRIM23 expression predicts cisplatin resistance in lung adenocarcinoma

Zhang

et al. 2020

Cancer Science

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Lung cancer is the leading cause of cancer-related deaths worldwide in both men and women. Lung adenocarcinoma (LUAD) is the fastest growing histological subtype of lung cancer, which develops from small airway epithelial and type II alveolar cells and shows different molecular biology features compared to other types. 1 Although progress has been made in the targeted treatment of LUAD, largely due to the development of small-molecule tyrosine kinase inhibitors (TKI) against epidermal growth factor receptor, anaplastic lymphoma receptor AbstractThe tripartite motif containing 23 (TRIM23) gene is a member of the tripartite motif (TRIM) family that participates in many pathophysiological processes. However, the role of TRIM23 in lung adenocarcinoma (LUAD) remains unclear. In the present study, TRIM23 was first screened by next-generation sequencing between the cisplatin (DDP)-resistant A549/DDP cell line and the parental A549 cell line, combined with integrated analysis of the Gene Expression Omnibus (GEO) data (E-GEOD-43493 and E-GEOD-43494). The expression of TRIM23 was then verified to be upregulated in the DDP-resistant LUAD cells and tissues. The knockdown of TRIM23 expression in A549/DDP cells caused increased apoptosis, decreased IC 50 values of DDP, NF-κB nuclear translocation, inhibition of cell proliferation in vitro and in vivo, inhibition of GLUT1/3 expression, glucose uptake, and lactate and ATP production. TRIM23 overexpression resulted in the opposite effects in A549 cells. In addition, the inhibition of proliferation in A549 cells caused by NF-κB signaling inhibitor PTDC or glycolysis inhibitor 3-BrPA could be weakened by TRIM23 overexpression. Furthermore, immunohistochemical analysis revealed that TRIM23 was upregulated in 46.1% (70/152) of LUAD cases, and elevated TRIM23 expression was correlated with high expressionof NF-κB, poor cellular differentiation, and adverse overall survival (OS) and diseasefree survival (DFS). In conclusion, our study demonstrates that TRIM23 acts as an oncogene in LUAD and promotes DDP resistance by regulating glucose metabolism via the TRIM23/NF-κB/ GLUT1/3 axis. K E Y W O R D Sglycolysis, lung adenocarcinoma, NF-κB, resistance, TRIM23

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“…NF-kB (transcripton factor nuclear kappa B) is an important mediator that acts in the chronic inflammaton [37]. NF-kB was highly expressed in ovarian cancer and related to ovarian cancer progression [38,39] . Immunotherapies attenuate the levels of nuclear factor kappa B, reduce cell dynamics and effectively target the TLR-related downstream molecules, eliciting a protective effect against chemoresistance [40].…”

Section: Discussionmentioning

confidence: 99%

Low expression of NCALD is associated with chemotherapy resistance and poor prognosis in epithelial ovarian cancer

Feng

2020

J Ovarian Res

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Background: Low expression of NCALD(neurocalcin delta) in peripheral blood of ovarian cancer patients predicts poor prognosis. However, the molecular mechanism of NCALD in ovarian cancer and its relationship with chemotherapy outcomes is unclear. The aim of this study was to investigate the potential signaling pathways of NCALD and to evaluate its ability to predict chemotherapy outcomes and prognosis. Methods: High-throughput RNA sequencing data were downloaded from TCGA. GSEA explored the potential signaling pathways of NCALD. The expression of NCALD in chemotherapy sensitive and chemotherapy resistant ovarian cancer patients was detected by TCGA data and clinical samples. ROC analysis confirmed the ability of NCALD to predict chemotherapy outcomes. The association between NCALD expression and prognosis in ovarian cancer patients was assessed using Kaplan-Meier plotter. Results: In patients with NCALD overexpression, genes expression related to ERK1 / 2 signaling pathway, NF-kappaB signaling pathway, TGF-β signaling pathway and immune response pathway was increased, especially ERK1 / 2 signaling pathway. The expression of NCALD in chemoresistant patients was significantly lower than chemosensitive patients. In TCGA data and immunohistochemical samples, the AUC of NCALD expression predicting chemotherapy outcome was 0.59 and 0.64, respectively. In clinical samples, low expression of NCALD was associated with poor OS and PFS. Conclusions: NCALD may activate the ERK1 / 2 signaling pathway in ovarian cancer. As a new biomarker of chemotherapy sensitivity, NCALD was significantly down-regulated in chemotherapy resistance ovarian cancer patients. Low expression of NCALD in ovarian cancer is associated with poor OS and PFS. In the future, further research will be needed on the potential mechanism and clinical application value of NCALD in ovarian cancer.

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TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway

Cited by 72 publications

References 28 publications

Tripartite motif containing 35 contributes to the proliferation, migration, and invasion of lung cancer cellsin vitroandin vivo

Tripartite motif containing 35 contributes to the proliferation, migration, and invasion of lung cancer cellsin vitroandin vivo

Elevated TRIM23 expression predicts cisplatin resistance in lung adenocarcinoma

Low expression of NCALD is associated with chemotherapy resistance and poor prognosis in epithelial ovarian cancer

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