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USP22 activates MYC. 29 / 32
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"In addition, USP22 expression was shown to increase the abundance of c-Myc and the androgen receptor itself [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Furthermore, it has been reported that USP22 positively regulates c-Myc and promotes tumorigenic activity in human breast cancer (22)."
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"48 Consistent with the results of the present study, USP22 has been shown to increase c-Myc stability via deubiquitination to enhance growth and colony formation of BC cells (T47D and MCF7 cells)."
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"21 USP22 overexpression accelerated c‐Myc/NRasGV12‐induced HCC in this study."
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"USP22 depletion in the lung cancer cells decreases the transcriptional ability of Myc [4]."
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"Decreased levels of USP22 reduce the ability of c-MYC, which can stimulate activation of AP4 to directly or indirectly induce EMT [XREF_BIBR], activating the transcription of its targets [XREF_BIBR, XREF_BIBR]."
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"61 In contrast, c-Myc promotes apoptosis and accelerates cell turnover during cellular carcinogenesis, thereby promoting the progression of cells toward increasingly malignant phenotypes.73 Therefore, it is hypothesized that USP22 promotes cancer progression in BC cells by stabilizing c-Myc to promote apoptosis."
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"In this study, we found that USP22 overexpression induces c-myc upregulation in both SGC7901 cells and tumor tissue, consistent with previous reports."
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"Taken together, USP22 accelerates c‐Myc/NrasGV12‐induced tumorigenesis and promotes tumor progression through an FKBP12/mTORC1/autophagy positive feedback loop in HCC cells."
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"Interestingly, a pioneer study from Kim et al. showed for the first time that USP22 promotes breast cancer by stabilizing the proto-oncogene c-Myc [37]."
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"Deubiquitinating enzyme USP22 positively regulates c-Myc stability and tumorigenic activity in mammalian and breast cancer cells."
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"Using conditional expression of the c- myc and p53 transcriptional activators, Zhang et al. (2008) find that USP22 knockdown reduces transcriptional activation of all c- myc and of most p53 target gen[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Evidently, HnRNPA1 is a downstream transcription regulator of c-Myc (proto-oncogene) whereas USP22 positively regulates c-Myc stability and promotes tumorigenesis [XREF_BIBR, XREF_BIBR]."
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"Our data revealed that knockdown of USP22 decreased the expression of stemness related genes Sox2 and CD133, redox related genes Nrf2 and Sirt1, and quiescence related genes PP2A and c-Myc in GSCs und[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Indeed, USP22 depletion reduces transformation of c-Myc and plays an important role in cell cycle progression and anchorage-independent growth [72]."
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"As presented in Fig. 2 A–B , knockdown of USP22 inhibited the expression of stemness related genes Sox2 and CD133, redox related genes Nrf2 and Sirt1, and quiescence related genes PP2A and c-Myc."
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"USP22 is a functional mediator necessary for MYC to promote cancer and can increase the stability and tumorigenic activity of MYC in cancer cells (65, 66)."
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"Furthermore, overexpression of USP22 stimulates breast cancer cell growth and colony formation, and increases c-Myc tumorigenic activity."
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"In conclusion, the present study reveals that USP22 in breast cancer cell lines increases c-Myc stability through c-Myc deubiquitination, which is closely correlated with breast cancer progression."
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"C-Myc abundance is also indirectly increased by the activity of USP22 on its substrate SIRT1, a NAD dependent protein deacetylase [XREF_BIBR] (see Section 7), but this is not observed in all cell types [XREF_BIBR]."
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"USP22 increases the stability and tumorigenic activity of c-Myc in breast cancer cells [30]."
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"Studies herein suggest that USP22 mediated MYC regulation in PCa is likely gene selective, based on USP22 increasing gene expression of AR/MYC co-regulated target (ODC) but not of multiple MYC targets."
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"While these outcomes could occur via USP22 mediated MYC and CyclinD2 and/or BMI-1-mediated modulation, AR activity promotes tumorigenesis in several of these tumor types, including bladder, HCC and breast carcinoma."
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"USP22 increased c-Myc stability via deubiquitination in breast cancer cells."
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"USP22 positively regulates c-Myc, androgen receptor, and HIF-1α actions to promote breast cancer, prostate cancer, and HCC progression [16, 53, 54]."
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"Deubiquitinating enzyme USP22 positively regulates c-Myc stability and tumorigenic activity in mammalian and breast cancer cells."
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"2.1 Overexpression of Usp22 accelerates c-Myc/NRasGV12-induced HCC in mice."
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"Furthermore, overexpression of USP22 stimulates breast cancer cell proliferation and aggregation and increases c-MYC tumorigenic activity (65)."
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"Moreover, USP37 and USP22 have been shown to increase c-Myc stability via blockade of proteasomal degradation ( Kim et al., 2017 ; Pan et al., 2015 )."
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