&lt;p&gt;Downregulation of USP34 Inhibits the Growth and Migration of Pancreatic Cancer Cells via Inhibiting the PRR11&lt;/p&gt;

Lin, Changjie; Xia, Jing; Gu, Zhiwei; Meng, Yunpeng; Gao, Dongliang; Wei, Shaohua

doi:10.2147/ott.s228857

Cited by 12 publications

(17 citation statements)

References 33 publications

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“…Mutation of the uncharacterized F-box protein FBXO8 renders cells resistant to the vesicular transport inhibitor brefeldin A, consistent with the presence of a Sec7-like domain in FBXO8 (Esmon et al, 1981;Misumi et al, 1986;Stevens et al, 1982). We find that loss of the poorly studied E3 RNF25 causes cells to be exquisitely sensitive to MMS (Figure 1 Single studies have implicated USP34 in cell migration, cell survival, BMP signaling, heart disease, EMT and stem cell maintenance, NF-kB and Wnt signaling, and the DNA damage response (Guo et al, 2018;Lin et al, 2020;Lui et al, 2011;Oh et al, 2017;Sy et al, 2013). Thus, while many genes have been suggested to have associations with the DNA damage response, our unbiased approach helps to identify those, like USP34, that have significant and specific roles in this area of biology.…”

Section: Discussionsupporting

confidence: 76%

A comprehensive phenotypic CRISPR-Cas9 screen of the ubiquitin pathway uncovers roles of ubiquitin ligases in mitosis

et al. 2021

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Section: Discussionsupporting

confidence: 76%

A comprehensive phenotypic CRISPR-Cas9 screen of the ubiquitin pathway uncovers roles of ubiquitin ligases in mitosis

et al. 2021

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“…We also found that MeCP2 binds to genomic regions devoid of CpG methylation such as for USP34, MGAM, GMDS, SLC45A4, SSU72, CAPN2 and PLXN2 ( Figures S1B–C ). Similarly, while these are novel targets of MeCP2, many have been implicated in diverse cancers ( 67 , 71 , 88 – 92 ). This further shows the complexity of MeCP2 binding across the genome.…”

Section: Resultsmentioning

confidence: 99%

Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications

et al. 2020

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Abnormal regulation of DNA methylation and its readers has been associated with a wide range of cellular dysfunction. Disruption of the normal function of DNA methylation readers contributes to cancer progression, neurodevelopmental disorders, autoimmune disease and other pathologies. One reader of DNA methylation known to be especially important is MeCP2. It acts a bridge and connects DNA methylation with histone modifications and regulates many gene targets contributing to various diseases; however, much remains unknown about how it contributes to cancer malignancy. We and others previously described novel MeCP2 post-translational regulation. We set out to test the hypothesis that MeCP2 would regulate novel genes linked with tumorigenesis and that MeCP2 is subject to additional post-translational regulation not previously identified. Herein we report novel genes bound and regulated by MeCP2 through MeCP2 ChIP-seq and RNA-seq analyses in two breast cancer cell lines representing different breast cancer subtypes. Through genomics analyses, we localize MeCP2 to novel gene targets and further define the full range of gene targets within breast cancer cell lines. We also further examine the scope of clinical and pre-clinical lysine deacetylase inhibitors (KDACi) that regulate MeCP2 post-translationally. Through proteomics analyses, we identify many additional novel acetylation sites, nine of which are mutated in Rett Syndrome. Our study provides important new insight into downstream targets of MeCP2 and provide the first comprehensive map of novel sites of acetylation associated with both pre-clinical and FDA-approved KDACi used in the clinic. This report examines a critical reader of DNA methylation and has important implications for understanding MeCP2 regulation in cancer models and identifying novel molecular targets associated with epigenetic therapies.

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“…In pancreatic cancer, silence of USP34 induced cell apoptosis, and obviously suppressed cell proliferation and migration by downregulating PRR11 and p-p38 expression. 9 Another paper also showed that overexpression of USP34 could promote pancreatic cancer cell proliferation and migration by increasing the expression of p-AKT and p-PKC. 10 Additionally, USP34 could stabilize axin protein, and promote β-cateninmediated transcription.…”

Section: Introductionmentioning

confidence: 99%

The deubiquitinase USP34 stabilizes SOX2 and induces cell survival and drug resistance in laryngeal squamous cell carcinoma

Dai

Yuan

Cao³

2020

The Kaohsiung J of Med Scie

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Recent studies showed that the deubiquitinase ubiquitin‐specific protease 34 (USP34) was involved in the tumorigenesis of several tumors, but its function and mechanism are still unclear in laryngeal squamous cell carcinoma (LSCC). In this study, we found that USP34 and SOX2 were elevated in LSCC tumor tissues, and we also found that USP34 expression was positively correlated with SOX2 expression. Our further studies showed that USP34 regulated the protein level of SOX2 in LSCC cells, but not the mRNA level, which suggested that USP34 stabilized SOX2. Moreover, USP34, as a deubiquitinase, could interact with SOX2, and reduce the polyubiquitination of SOX2. In addition, knockdown of USP34 could significantly inhibit LSCC cell growth, but overexpression of SOX2 could reverse this effect. Finally, we also found that USP34 and SOX2 were upregulated in cisplatin‐resistant LSCC cells, but knockdown of USP34 could enhance the drug sensitivity of cisplatin in the resistant cells. Collectively, targeting USP34/SOX2 axis may be a promising strategy for the treatment of LSCC.

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<p>Downregulation of USP34 Inhibits the Growth and Migration of Pancreatic Cancer Cells via Inhibiting the PRR11</p>

Cited by 12 publications

References 33 publications

A comprehensive phenotypic CRISPR-Cas9 screen of the ubiquitin pathway uncovers roles of ubiquitin ligases in mitosis

A comprehensive phenotypic CRISPR-Cas9 screen of the ubiquitin pathway uncovers roles of ubiquitin ligases in mitosis

Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications

The deubiquitinase USP34 stabilizes SOX2 and induces cell survival and drug resistance in laryngeal squamous cell carcinoma

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