IndraLab

Statements


USP45 activates MYC. 8 / 8
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"Further, USP45 overexpressing can upregulate MYC, and this overexpressing can significantly enhance cancer development, cancer cell stemness and drug resistance."

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"Furthermore, we have found that USP45 inhibition with a natural small molecule promoted MYC degradation and, in turn, reduced MYC-mediated stemness and drug resistance in cervical cancer."

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"We found that USP45 overexpressing significantly upregulated MYC (Figure 1A), and USP45 inhibition with the serval siRNAs significantly decreased MYC (Figure 1B)."

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"The MYC decrease by USP45 inhibition with siRNA was reversed by overexpression of USP45 (Figure 1C) or by the addition of the proteasome inhibitor MG132 (Figure 1D)."

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"MYC regulation by USP45 was dependent on its DUB activity (Figure 1E), and the USP45 resulted in MYC elevation in a dose-dependent manner (Figure 1F), while its C199A mutant did not have any impact on the MYC level."

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"Further, we have discovered that increased USP45 expression significantly promoted cervical cancer cell proliferation, stemness and drug resistance, while USP45-enhanced MYC stability facilitated only stemness and drug resistance."

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"Furthermore, through RT-qPCR and Western blot, we confirm that USP45 overexpression up-regulated the mRNA and protein levels of MYC and ATAD2, while USP45 knockdown down-regulated MYC and ATAD2."

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"USP45 has been demonstrated to modulate the stability of Spindly and MYC proteins through deubiquitination (Conte et al., 2018; Tu et al., 2023)."