<scp>USP</scp>26 regulates <scp>TGF</scp>‐β signaling by deubiquitinating and stabilizing <scp>SMAD</scp>7

Lui, Sarah Kit Leng; Iyengar, Prasanna Vasudevan; Jaynes, Patrick; Isa, Zul Fazreen Bin Adam; Pang, Brendan; Tan, Tuan Zea; Eichhorn, Pieter J.A.

doi:10.15252/embr.201949618

Cited by 4 publications

(8 citation statements)

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“…The journal is therefore retracting these panels. The authors have outlined the specific issues in their correspondence , published alongside this notice.…”

Section: Journal Statementmentioning

confidence: 99%

“…The authors have supplied a new analysis of the REMBRANDT database using glioblastoma patients only, and the journal has decided to retract and replace these panels. Further discussion on the re‐analysis is available in the correspondence co‐published with this notice .…”

Section: Journal Statementmentioning

confidence: 99%

“…The authors detail their response to Zhu et al in the correspondence published alongside this notice.…”

Section: Journal Statementmentioning

confidence: 99%

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USP26 regulates TGF‐β signaling by deubiquitinating and stabilizing SMAD7

Lui¹,

Iyengar²,

Jaynes³

et al. 2019

EMBO Reports

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“…The journal is therefore retracting these panels. The authors have outlined the specific issues in their correspondence , published alongside this notice.…”

Section: Journal Statementmentioning

confidence: 99%

Section: Journal Statementmentioning

confidence: 99%

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USP26 regulates TGF‐β signaling by deubiquitinating and stabilizing SMAD7

Lui¹,

Iyengar²,

Jaynes³

et al. 2019

EMBO Reports

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“…Leng Lui et al [3]). These findings are in agreement with those presented by Ware and colleagues, where they indicate that, "Our findings agree with the authors reported trend with low USP26 expression conferring to poorer prognosis, although the effect on survival is minor and the clinical relevance remains unclear" [2].…”

Section: Fig 5d In Kitmentioning

confidence: 99%

“…All Kaplan-Meier curves are extrapolated from datasets based on median threshold levels (high versus low). [3]). Taken together, these data are consistent with our original conclusions that deregulation of TGFb pathway components, resulting in the hyperactivation of the TGF-b pathway, may act as biomarkers for poor clinical outcome in glioblastoma.…”

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Response to: USP26 regulates TGF‐β signalling by deubiquitinating and stabilizing SMAD7; not applicable in glioblastoma

et al. 2019

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that the Kaplan-Meier analysis shown in Figs 5D and EV5B-E of our original study was based on a mixture of glioblastoma, oligodendroglioma and astrocytoma patients [1,2]. Since these tumours are clinically and molecularly distinct, the relevance of USP26 and the tested TGF-b pathway components to the survival of glioblastoma patients was questioned. Moreover, we were alerted to an error in the statistical analysis in Fig 5A. During the evaluation of the REMBRANDT (REpository for Molecular BRAin Neoplasia DaTa) database (http://www.betastasis.com/ glioma/rembrandt/kaplan_meier_survival_ curve/), we did not realise that the dataset used not only included glioblastoma samples, but also oligodendroglioma and astrocytoma samples. As such, our initial analysis of USP26 expression included all three tumour types and Figs 5D and EV5B-E are thus incorrectly labelled.We have now re-evaluated the expression of USP26 in specifically the REMBRANDT glioblastoma dataset and included further analysis of the TCGA (cBioPortal) glioblastoma datasets. In line with our previous results, we demonstrate that low USP26 expression is associated with poorer overall survival in glioblastoma, at the median threshold (high vs low), showing statistical significance with an overall P-value of 0.0259 (REMBRANDT) (new Fig 5D in Kit Leng Lui et al [3]). These findings are in agreement with those presented by Ware and colleagues, where they indicate that, "Our findings agree with the authors reported trend with low USP26 expression conferring to poorer prognosis, although the effect on survival is minor and the clinical relevance remains unclear" [2]. Furthermore, we have now analysed USP26 expression in the most recent TCGA GBM cohort from cBioPortal (TCGA GBM, mRNA RNA-seq v2 RSEM data, z score 2 threshold 1.0, n = 166). Again, we demonstrate that low USP26 expression correlates with poorer overall survival in glioblastoma patients with a significant P-value of 0.0153 (Fig 1). We have now also included new analyses correlating the expression of USP26 in astrocytoma and oligodendroglioma. We demonstrate that USP26 does not associate with patient survival in oligodendroglioma or astrocytoma (Fig 2A and B). These data are therefore consistent with the conclusions in our original manuscript that loss of USP26 confers poor prognosis in glioblastoma.In a similar fashion, we attempted to correlate TGFBRI, TGFBRII, TGFBRIII, and SMAD7 expression with survival in glioblastoma. As noted, we did not realise that the REMBRANDT dataset was comprised of glioblastoma and lower-grade gliomas. As such, results pertaining to these analyses were also mislabelled. As has been demonstrated in a number of recent publications, high TGF-b activity is a poor prognostic factor in glioblastoma; therefore, we reasoned that deregulated TGFBRI, TGFBRII, TGFBRIII, and SMAD7 expression may also correlate with lower survival outcome. While our new analysis of the REMBRANDT database does not show a correlation between lower patient survival and high TGFBRI, TGFBRII, or TGFBRII...

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Identification of ubiquitin-specific protease 32 as an oncogene in glioblastoma and the underlying mechanisms

Chen

et al. 2022

Sci Rep

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Glioblastoma (GBM) patients present poor prognosis. Deubiquitination by deubiquitinating enzymes (DUBs) is a critical process in cancer progression. Ubiquitin-specific proteases (USPs) constitute the largest sub-family of DUBs. Evaluate the role of USP32 in GBM progression and provide a potential target for GBM treatment. Clinical significance of USP32 was investigated using Gene Expression Omnibus databases. Effects of USP32 on cell growth and metastasis were studied in vitro and in vivo. Differentially expressive genes between USP32-knockdown U-87 MG cells and negative control cells were detected using RNA sequencing and used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomic pathway enrichment analyses. Finally, RT-qPCR was used to validate the divergent expression of genes involved in the enriched pathways. USP32 was upregulated in GBM patients, being correlated to poor prognosis. USP32 downregulation inhibited cell growth and metastasis in vitro. Furthermore, USP32 knockdown inhibited tumorigenesis in vivo. In addition, UPS32 was identified as a crucial regulator in different pathways including cell cycle, cellular senescence, DNA replication, base excision repair, and mismatch repair pathways. USP32 acts as an oncogene in GBM through regulating several biological processes/pathways. It could be a potential target for GBM treatment.

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USP26 regulates TGF‐β signaling by deubiquitinating and stabilizing SMAD7

Cited by 4 publications

References 4 publications

USP26 regulates TGF‐β signaling by deubiquitinating and stabilizing SMAD7

USP26 regulates TGF‐β signaling by deubiquitinating and stabilizing SMAD7

Response to: USP26 regulates TGF‐β signalling by deubiquitinating and stabilizing SMAD7; not applicable in glioblastoma

Identification of ubiquitin-specific protease 32 as an oncogene in glioblastoma and the underlying mechanisms

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