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USP17L2 activates Carcinogenesis. 7 / 7
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"Moreover, an in vivo assay showed that DUB3 deficiency inhibited HCC tumorigenesis through stabilization of MAGEA3.Palbociclib, a selective CDK4/6 inhibitor, has been reported to inhibit DUB3 activity in breast cancer.29 34 Interestingly, we found that palbociclib treatment also efficiently inactivated DUB3 in HCC cells and consequently shortened the half-life, increased the polyubiquitination and promoted the protein degradation of MAGEA3."
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"Moreover , the in vivo animal models revealed that USP17 suppression reduced tumorigenesis and growth ."
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"Moreover, DUB3 knockout attenuates HCC tumorigenesis in vivo, which can be rescued by restoration of MAGEA3."
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"Suppression of USP17 reduced tumorigenesis and progression of NSCLC in vivo ."
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"Taken together , our study showed that USP17 promotes tumorigenesis and invasion through regulation of MMPs ( MMP3 and MMP9 ) in NSCLC cells and provides a promising approach for NSCLC treatment and prevention ."
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"DUB3 has been reported to promote cell proliferation in various cancers, including oral squamous cell carcinoma (OSCC),41 non-small cell lung cancer,33 gastric cancer19 and prostate cancer,42 suggesting that DUB3 may serve as an oncogenic driver to promote tumorigenesis."
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"Suppression of Ubiquitin-Specific Peptidase 17 ( USP17 ) Inhibits Tumorigenesis and Invasion in Non-Small Cell Lung Cancer Cells USP17 PROMOTES TUMORIGENESIS AND METASTASIS IN NSCLC ZHANG , YUAN , AND ZHENG Recently , deubiquitinating enzymes ( DUBs ) are emerging as new regulators in cancer progression ."
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