TRIM24 as an independent prognostic biomarker for prostate cancer

Offermann, Anne; Roth, Doris; Hupe, Marie C.; Hohensteiner, Silke; Becker, Finn; Joerg, Vincent; Carlsson, Jessica; Kuempers, Christiane; Ribbat‐Idel, Julika; Tharun, Lars; Sailer, Verena; Kirfel, Jutta; Svensson, Maria A.; Andrén, Ove; Lubczyk, Verena; Kuefer, Rainer; Merseburger, Axel S.; Perner, Sven

doi:10.1016/j.urolonc.2019.05.006

Cited by 19 publications

(24 citation statements)

References 21 publications

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“…5 High levels of expression of TRIM24 have frequently been detected in tumor tissues and have been associated with clinical stage, lymphatic metastasis, and low survival rate. 9,10 Elevated levels of TRIM24 expression promote the tumor growth and metastasis as well as chemoresistance by affecting various signaling pathways. [11][12][13] The oncogenic function of TRIM24 has been demonstrated in a variety of other cancer types, [14][15][16][17] making it as an attractive target for further study.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling

Xin

Shi

et al. 2020

Hum Exp Toxicol

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Tripartite motif-containing protein 24 (TRIM24) has currently emerged as a crucial cancer-related gene present in a wide range of human cancer types. However, the involvement of TRIM24 in acute myeloid leukemia (AML) has not been well investigated. The present study aims to investigate the significance, cellular function, and potential regulatory mechanism of TRIM24 in AML. We found that TRIM24 expression was significantly upregulated in AML compared with normal tissues. AML patients with low expression of TRIM24 had higher survival rates than those expressing TRIM24 at higher levels. High expression of TRIM24 was also detected in AML cells and its knockdown markedly restricted proliferation and promoted apoptosis in AML cells. Further investigation revealed that TRIM24 contributed to the regulation of Wnt/β-catenin signaling, which was associated with modulating the phosphorylation status of glycogen synthase kinase-3β (GSK-3β). Inactivation of GSK-3β partially reversed the TRIM24 knockdown-mediated antitumor effects observed in AML cells. Furthermore, knockdown of TRIM24 retarded the growth of AML-derived xenograft tumors in nude mice in vivo. Overall, these findings demonstrate that knockdown of TRIM24 impedes the AML tumor growth through the modulation of Wnt/GSK-3β/β-catenin signaling. These findings highlight the potential TRIM24 as an attractive anticancer target to treat AML.

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Section: Introductionmentioning

confidence: 99%

Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling

Xin

Shi

et al. 2020

Hum Exp Toxicol

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“…Meanwhile, lowlyexpressed miR-138-2-3p has been found in drugresistant non-small cell lung cancer patients [42]. As for TRIM24, it is a member of the tripartite motif (TRIM) family [20], and the oncogenic role of TRIM24 in carcinogenesis has been demonstrated in several cancer types [43][44][45]. Moreover, our study identified that inhibited miR-138-2-3p or promoted TRIM24 stimulated Wnt/β-catenin activation in glioma cells, which was in line with the previous studies [21,41].…”

Section: Discussionmentioning

confidence: 99%

“…We further determined tripartite motif-containing 24 (TRIM24) as an indirect target of NCK1-AS1 through the miR-138-2-3p sponge. TRIM24 is a member of the TRIM family with its oncogenic role being identified in prostate cancer [20]. In addition, TRIM24 has been suggested to promote cancer progression by triggering the Wnt/β-catenin signaling pathway [21,22].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Huang

et al. 2020

J Exp Clin Cancer Res

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Background: Glioma is a common brain malignancy with high mortality. The competing endogenous RNA (ceRNA) networks may play key roles in cancer progression. This study was conducted to probe the role of long noncoding RNA (lncRNA) NCK1-AS1 in glioma progression and the involved mechanisms.Methods: Microarray analyses were performed to explore the lncRNAs/miRNAs/genes with differential expression in glioma. NCK1-AS1 levels in glioma tissues and normal brain tissues, and in glioma cell lines and normal human glial cells were identified. The interactions among NCK1-AS1, miR-138-2-3p and TRIM24 were validated through luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Gain-and loss-of functions of NCK1-AS1, miR-138-2-3p and TRIM24 were performed to identify their roles in the behaviors of glioma cells. The activity of the Wnt/β-catenin pathway was measured. In vivo experiments were performed as well.Results: High expression of NCK1-AS1 was found in glioma tissues and cells, especially in U251 cells. Online predictions and the integrated experiments identified that NCK1-AS1 elevated the TRIM24 expression through sponging miR-138-2-3p, and further activated the Wnt/β-catenin pathway. Artificial silencing of NCK1-AS1 or upregulation of miR-138-2-3p led to inhibited proliferation, invasion and migration but promoted cell apoptosis of U251 cells, while up-regulation of TRIM24 reversed these changes, and it activated the Wnt/β-catenin pathway. The in vitro results were reproduced in in vivo experiments.Conclusions: Our study suggested that NCK1-AS1 might elevate TRIM24 expression and further activate the Wnt/βcatenin pathway via acting as a ceRNA for miR-138-2-3p. Silencing of NCK1-AS1 might inhibit the progression of glioma.

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“…Another example of successful siRNA treatment is the tripartite motif-containing protein 24 (TRIM24), a carcinogenesis factor capable of enhancing progression and viability of different cancers [ 79 , 80 ]. The strategy is based on suppressing TRIM24 in cancer therapy [ 81 ]. The treatment is based on in vitro and in vivo experiments showing that TRIM24-siRNA is effective in the eradication of PCa cells.…”

Section: Sirna Targets Signaling Pathways: Focus On Pca Therapymentioning

confidence: 99%

Progress in Delivery of siRNA-Based Therapeutics Employing Nano-Vehicles for Treatment of Prostate Cancer

et al. 2020

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Prostate cancer (PCa) accounts for a high number of deaths in males with no available curative treatments. Patients with PCa are commonly diagnosed in advanced stages due to the lack of symptoms in the early stages. Recently, the research focus was directed toward gene editing in cancer therapy. Small interfering RNA (siRNA) intervention is considered as a powerful tool for gene silencing (knockdown), enabling the suppression of oncogene factors in cancer. This strategy is applied to the treatment of various cancers including PCa. The siRNA can inhibit proliferation and invasion of PCa cells and is able to promote the anti-tumor activity of chemotherapeutic agents. However, the off-target effects of siRNA therapy remarkably reduce its efficacy in PCa therapy. To date, various carriers were designed to improve the delivery of siRNA and, among them, nanoparticles are of importance. Nanoparticles enable the targeted delivery of siRNAs and enhance their potential in the downregulation of target genes of interest. Additionally, nanoparticles can provide a platform for the co-delivery of siRNAs and anti-tumor drugs, resulting in decreased growth and migration of PCa cells. The efficacy, specificity, and delivery of siRNAs are comprehensively discussed in this review to direct further studies toward using siRNAs and their nanoscale-delivery systems in PCa therapy and perhaps other cancer types.

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TRIM24 as an independent prognostic biomarker for prostate cancer

Cited by 19 publications

References 21 publications

Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling

Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling

Long non-coding RNA NCK1-AS1 promotes the tumorigenesis of glioma through sponging microRNA-138-2-3p and activating the TRIM24/Wnt/β-catenin axis

Progress in Delivery of siRNA-Based Therapeutics Employing Nano-Vehicles for Treatment of Prostate Cancer

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