IndraLab

Statements

USP39 activates EGFR. 4 / 6
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"To verify whether the regulatory effect of USP39 was EGFR specific, ectopic expression of USP39 were performed in PC-3 and DU145 cells, which showed that overexpressed USP39 upregulated EGFR mRNA and protein levels, indicating that EGFR is a downstream target of USP39."
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"It was found in our previous study that USP39 knockdown could inhibit the abnormal proliferation of prostate cancer cells by inhibiting the splicing maturation and transcriptional prolongation of EGFR mRNA [16]."
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"We hypothesized that USP39 could up-regulate EGFR by increasing the pre-mRNA splicing."
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"The results demonstrated that the level of the 3 '-end of EGFR decreased (P = 0.0015) more sharply than that of the 5 '-end (P = 0.0069), and the ratio ofthe 3 '-end to 5 '-end levels was significant decreased (P = 0.0297), implying that knockdown of USP39 might inhibit the transcription elongation of EGFR, and might produce unstable EGFR mRNA fragments lacking the 3 '-UTR."
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