ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Yang, Haiyan; Palmbos, Phillip L.; Wang, Lidong; Kim, Evelyn H.; Ney, Gina M.; Liu, Chao; Prasad, J.K.; Misek, David E.; Yu, Xiaochun; Ljungman, Mats; Simeone, Diane M.

doi:10.1074/jbc.m115.665489

Cited by 19 publications

(16 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study reports that ATDC is essential for TP63‐regulated basal cancer invasive program . Moreover, ATDC exerts its oncogenic effect by promoting the radio‐resistance and chemo‐resistance of tumour cells . Consistent with these findings, our study demonstrated that ATDC was highly expressed in HCC cell, suggesting a potential oncogenic function of ATDC.…”

Section: Discussionsupporting

confidence: 90%

“…34 Moreover, ATDC exerts its oncogenic effect by promoting the radioresistance and chemo-resistance of tumour cells. [35][36][37] Consistent with these findings, our study demonstrated that ATDC was highly expressed in HCC cell, suggesting a potential oncogenic function of ATDC. Functional experiments showed that the knockdown of ATDC impeded the growth and invasion of HCC cells, while the overexpression of ATDC promoted HCC cell growth and invasion.…”

Section: Discussionsupporting

confidence: 88%

See 1 more Smart Citation

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK‐3β/Wnt/β‐catenin signalling

Xue

et al. 2019

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Accumulating evidence has suggested that the ataxia telangiectasia group D complementing (ATDC) gene is an emerging cancer‐related gene in multiple human cancer types. However, little is known about the role of ATDC in hepatocellular carcinoma (HCC). In this study, we aimed to investigate the expression level, biological function and underlying mechanism of ATDC in HCC. The expression of ATDC in HCC cells was detected by quantitative real‐time polymerase chain reaction and western blot analysis. Cell growth was determined by cell counting kit‐8 assay and colony formation assay. Cell invasion was assessed by Transwell invasion assay. The activation status of Wnt/β‐catenin signalling was evaluated by the luciferase reporter assay. Functional experiments showed that the silencing of ATDC expression significantly suppressed the growth and invasion of HCC cells, whereas the overexpression of ATDC promoted the growth and invasion of HCC cells in vitro. Moreover, we showed that ATDC overexpression promoted the phosphorylation of glycogen synthase kinase (GSK)‐3β and resulted in the activation of Wnt/β‐catenin signalling. Notably, the inhibition of GSK‐3β activity significantly abrogated the tumour suppressive effect of ATDC silencing, while the silencing of β‐catenin partially reversed the oncogenic effect of ATDC overexpression. Taken together, these findings reveal an oncogenic role of ATDC in HCC and show that the suppression of ATDC impedes the growth and invasion of HCC cells associated with the inactivation of Wnt/β‐catenin signalling. Our study suggests that ATDC may serve as a potential therapeutic target for HCC.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 88%

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK‐3β/Wnt/β‐catenin signalling

Xue

et al. 2019

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…A recent report showed that the interaction of TRIM29 phosphorylated at Ser550 with RNF8 upregulates DNA damage responses (DDR), including H2AX ubiquitination, 53BP1 phosphorylation, and formation of DNA damage foci [7] (Figure 1). Recently, we showed that TRIM29 is a histone-binding protein responsible for DDR and that TRIM29 interacts with BRCA1-associated surveillance complex, cohesion, DNA-PKcs, and components of Tat-interactive protein 60 (TIP60) complex by cross talk between histone modifications [8] (Figure 1).…”

Section: Trim29 As An Oncogenic Regulatormentioning

confidence: 99%

Early evidence for the role of TRIM29 in multiple cancer models

Hatakeyama

2016

Expert Opinion on Therapeutic Targets

View full text Add to dashboard Cite

“…However, a weak E3 ligase activity of TRIM29 mediated via B-box domain has recently been reported (15). In addition, following DNA damage, TRIM29 is phosphorylated and interacts with RNF8, an E3 ubiquitin ligase, which promotes DNA repair and cell survival (16). The TRIM family proteins are involved in a series of biological and physiological processes.…”

Section: Introductionmentioning

confidence: 99%

High expression of TRIM29 (ATDC) contributes to poor prognosis and tumor metastasis by inducing epithelial-mesenchymal transition in osteosarcoma

et al. 2017

View full text Add to dashboard Cite

Abstract. The association of TRIM29 overexpression with cancer progression and poor clinical prognosis has been reported in the context of several types of cancers. In the present study, we investigated the prognostic relevance of TRIM29 and its involvement in the progression of human osteosarcoma. To the best of our knowledge, this is the first study to demonstrate a major role of TRIM29 in osteosarcoma. Our results showed that the expression of TRIM29 in osteosarcoma tissues was much higher than that in normal bone tissues. Furthermore, TRIM29 expression was significantly correlated with tumor size, recurrence, metastasis and overall survival time. High expression of TRIM29 and presence of metastasis were independent predictors of poor prognosis in these patients. Both protein and mRNA expression of TRIM29 in osteosarcoma cell lines were significantly higher than those in osteoblast cell line, hFOB1.19. Moreover, the results indicated that TRIM29 promoted migration and invasive growth of osteosarcoma cells by inducing epithelial-mesenchymal transition. Therefore, ectopic expression of TRIM29 potentially contributes to metastasis and poor prognosis in patients with osteosarcoma. In summary, TRIM29 is a potential prognostic biomarker and a therapeutic target for patients with osteosarcoma.

show abstract

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Cited by 19 publications

References 31 publications

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK‐3β/Wnt/β‐catenin signalling

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK‐3β/Wnt/β‐catenin signalling

Early evidence for the role of TRIM29 in multiple cancer models

High expression of TRIM29 (ATDC) contributes to poor prognosis and tumor metastasis by inducing epithelial-mesenchymal transition in osteosarcoma

Contact Info

Product

Resources

About