IndraLab

Statements

USP22 activates Carcinogenesis. 6 / 6
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eidos
"In addition , we find that USP22 promotes de novo fatty acid synthesis and contributes to HCC tumorigenesis , however , this tumorigenicity is suppressed by inhibiting the expression of PPARgamma , ACLY , or ACC in in vivo tumorigenesis experiments ."
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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 [ 35,36 ] ."
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"Further , USP22 is shown to facilitate cell-cycle progression and colorectal tumorigenesis by targeting CCNB1 while in glioblastoma , USP22 promotes tumorigenesis via stabilizing KDM1A [ 89,90 ] ."
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"Together, these results support that USP22 promotes CRC cell proliferation and tumorigenesis by stabilizing FASN."
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"Together, these results suggest that FASN is stabilized by USP22 in colorectal cancer, and the dysregulated USP22/FASN axis is a important driver for tumorigenesis."
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"In addition, we find that USP22 promotes de novo fatty acid synthesis and contributes to HCC tumorigenesis, however, this tumorigenicity is suppressed by inhibiting the expression of PPARγ, ACLY, or ACC in in vivo tumorigenesis experiments."
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