Cancer-testis specific gene OIP5: a downstream gene of E2F1 that promotes tumorigenesis and metastasis in glioblastoma by stabilizing E2F1 signaling

Jiang, He; Zhao, Yuzu; Zhao, Erhu; Wang, Xianxing; Dong, Zhen; Chen, Yibiao; Yang, Liqun; Cui, Hongjuan

doi:10.1093/neuonc/noy037

Cited by 31 publications

(28 citation statements)

References 40 publications

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“…Previous studies have demonstrated that the binding of two proteins could result in altered expression level of one protein through regulating the ubiquitination level. He et al showed that OIP5 interacts with and stabilizes E2F1 by inhibiting its ubiquitination . According to a study by Chen et al, Smad6 and Tbx6 bind to each other, and Smad6 facilitates the ubiquitin‐mediated degradation of Tbx6 protein through recruitment of Smurf1, a ubiquitin E3 ligase .…”

Section: Discussionmentioning

confidence: 99%

5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

et al. 2019

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Serotonin and its receptors have been shown to play critical regulatory roles in cancer biology. Nevertheless, the contributions of 5‐hydroxytryptamine 1D (5‐HT1D), an indispensable member of the serotonergic system, to hepatocellular carcinoma (HCC) remain unknown. The present study demonstrated that the 5‐HT1D expression level was significantly up‐regulated in HCC tissues and cell lines. The 5‐HT1D expression level was closely correlated with unfavorable clinicopathological characteristics. Survival analyses show that elevated 5‐HT1D expression level predicts poor overall survival and high recurrence probability in HCC patients. Functional studies revealed that 5‐HT1D significantly promoted HCC proliferation, epithelial‐mesenchymal transition, and metastasis in vitro and in vivo. Mechanistically, 5‐HT1D could stabilize PIK3R1 by inhibiting its ubiquitin‐mediated degradation. The interaction between 5‐HT1D and phosphoinositide‐3‐kinase regulatory subunit 1 (PIK3R1) enhanced the expression of FoxO6 through the PI3K/Akt signaling pathway; FoxO6 could also be directly transcriptionally activated by 5‐HT1D in an Akt‐independent manner. MicroRNA‐599 was found to be an upstream suppressive modulator of 5‐HT1D. Additionally, 5‐HT1D could attenuate tryptophan hydroxylase 1 expression through the PI3K/Akt/cut‐like homeobox 1 axis in HCC. Conclusion: Herein, we uncovered the potent oncogenic effect of 5‐HT1D on HCC by interacting with PIK3R1 to activate the PI3K/Akt/FoxO6 pathway, and provided a potential therapeutic target for HCC.

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Section: Discussionmentioning

confidence: 99%

5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

et al. 2019

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“…The expression of NUSAP1 in patients was analyzed using the R2: Genomics Analysis and Visualization Platform database as described previously. 44 Western blot analysis Western blotting was performed as described previously. 43 Plasmids, transfection, and infection NUSAP1-specific short hairpin RNAs (shRNAs) were purchased from Sigma-Aldrich and then cloned into the PLKO.1 vector.…”

Section: Patient Data Analysismentioning

confidence: 99%

“…43 Flow cytometry analysis Flow cytometry analysis was performed as described previously. 44 Comet assay A comet assay to detect DNA damage in cells was performed following the manufacturer's instructions. Briefly, cells were harvested and counted to 1 × 10 5 /ml, and mixed with molten LM agarose at a ratio of 1:10 (V/V) and immediately pipetted into 50 µl of mixture onto CometSlide.…”

Section: Patient Data Analysismentioning

confidence: 99%

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NUSAP1 potentiates chemoresistance in glioblastoma through its SAP domain to stabilize ATR

Zhao

Jiang

et al. 2020

Sig Transduct Target Ther

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NUSAP1, which is a microtubule-associated protein involved in mitosis, plays essential roles in diverse biological processes, especially in cancer biology. In this study, NUSAP1 was found to be overexpressed in GBM tissues in a grade-dependent manner compared with normal brain tissues. NUSAP1 was also highly expressed in GBM patients, dead patients, and GBM cells. In addition, NUSAP1 was found to participate in cell proliferation, apoptosis, and DNA damage in GBM cells. Ataxia telangiectasia and Rad3related protein (ATR) are a primary sensor of DNA damage, and ATR is also a promising target in cancer therapy. Here, we found that NUSAP1 positively regulated the expression of ATR. Mechanistically, NUSAP1 suppressed the ubiquitin-dependent proteolysis of ATR. The SAP (SAF-A/B, Acinus, and PIAS) domain is a common motif of many SUMO (small ubiquitin-like modifier) E3 ligases, and this domain is involved in substrate recognition and ligase activity. This study further demonstrated that the SAP domain of NUSAP1 promoted the sumoylation of ATR, and thereby antagonized the ubiquitination of ATR. These results suggest that NUSAP1 stabilizes ATR by sumoylation. Moreover, NUSAP1 potentiated chemotherapeutic resistance to temozolomide (TMZ) and doxorubicin (DOX) through its SAP domain. Overall, this study indicates that NUSAP1 is a promising therapeutic target in GBM.

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“…no. RG088S; Beyotime Institute of Biotechnology) (28). The promotor activity was normalized to Renilla luciferase activity.…”

Section: Dual-luciferase Assay and Promoter Analysismentioning

confidence: 99%

FOXO3a‑SIRT6 axis suppresses aerobic glycolysis in melanoma

Dong

Yang

et al. 2020

Int J Oncol

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Melanoma, the most aggressive human skin tumor, has a very short survival time, and there are currently no effective treatments. Alterations in cell metabolism, such as enhanced aerobic glycolysis, have been identified as hallmarks of cancer cells. In the present study, bioinformatics studies using online databases revealed that FOXO3a expression was lower in melanoma tissues compared with normal tissues and nevus. Additionally, Kaplan-Meier analysis showed that high expression of FOXO3a predicted an improved prognosis for patients with melanoma. Furthermore, Pearson correlation analysis indicated that the expression of FOXO3a was positively correlated with SIRT6 expression and negatively correlated with the expression levels of a number of glycolysis-associated genes. Chromatin immunoprecipitation and luciferase assays showed that FOXO3a was enriched in the SIRT6 promoter region and promoted its transcription. Then, SIRT6 was overexpressed in FOXO3a-knockdown MV3 cells and downregulated in FOXO3a-overexpressing MV3 cells by using lentivirus-mediated stable infection. The results showed that SIRT6 knockdown or overexpression rescued the effects of FOXO3a overexpression or knockdown, respectively, on glycolysis, as determined by glucose uptake, glucose consumption and lactate production assays, the expression of glycolytic genes and glucose stress flux tests. SIRT6 overexpression also suppressed FOXO3a knockdown-induced tumor growth in a mouse model. The present findings indicated that the FOXO3a-SIRT6 regulatory axis inhibited glucose metabolism and tumor cell proliferation in melanoma, and provided novel insight into potential therapeutic strategies to treat this disease.

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Cancer-testis specific gene OIP5: a downstream gene of E2F1 that promotes tumorigenesis and metastasis in glioblastoma by stabilizing E2F1 signaling

Abstract: Collectively, our findings demonstrate that OIP5 promotes glioblastoma progression and metastasis, suggesting that OIP5 is a potential target for anticancer therapy.

Cited by 31 publications

References 40 publications

5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

NUSAP1 potentiates chemoresistance in glioblastoma through its SAP domain to stabilize ATR

FOXO3a‑SIRT6 axis suppresses aerobic glycolysis in melanoma

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