IndraLab

Statements

USP17L2 activates Neoplasm Invasiveness. 9 / 9
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"USP17 promotes proliferation and invasion through PI3K / AKT activation in NSCLC Consistent with the findings from the USP17-OE cells , knock-down ( KD ) of USP17 decreased the protein expression levels of p-AKT and p-PI3K in NSCLC cells ( NC vs. KD , P < 0.0001 ; Fig. 6A-F ) ."
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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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"DUB3 (official symbol USP17L2) was shown to promote breast cancer invasion and metastasis via stabilizing Snail1 in a CDK4/6 activity-dependent manner ."
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"Dub3 mediates migration, invasion and CSC like properties of breast cancer cells."
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"Dub3 is overexpressed in breast cancer; knockdown of Dub3 resulted in Snail1 destabilization, suppressed EMT and decreased tumour cell migration, invasion, and metastasis."
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"Dub3 inhibition suppresses breast cancer invasion and metastasis by promoting Snail1 degradation."
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"Dub3 inhibition suppresses breast cancer invasion and metastasis by promoting Snail1 degradation."
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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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"Furthermore, we demonstrated that Dub3 promoted migration, invasion and CSC like properties of breast cancer cells."
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