IndraLab

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"The results showed that overexpression of USP44 inhibited malignant cell phenotypes in vitro and suppressed tumor growth and lung metastasis in vivo, while its downregulation had the opposite effects."

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"Additionally, several tumor suppressors, including SFRP1, HOPX, SHISA3, and USP44, are reported to be silenced by DNA methylation and be involved in regulating NPC metastasis and treatment resistance [15–18], suggesting that DNA methylation dysregulation is an essential event in NPC.The ubiquitin-proteasome system plays a pivotal role in regulating protein degradation, functionality, and subcellular trafficking to maintain cellular homeostasis [19]."

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"However, Chen et al (83) reported contrary results and suggested that USP44 acts as a tumor suppressor in breast cancer to limit tumor progression."

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"These data reveal the requirement for highly regulated ubiquitin addition and removal in the recognition and repair of helix-distorting DNA damage and identify another mechanism by which USP44 protects genomic integrity and prevents tumors ."

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"We examined the effect of a nuclear-residing Gli1 mutant on USP44 overexpression-mediated tumor inhibition."

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"On the contrary, due to the tumor-suppressing role of Fructose-1,6-bisphosphatase (FBP1), the deubiquitinating role of USP44 stabilizing FBP1 suppressed tumor proliferation, metastasis and increased g[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"For example, USP44 was demonstrated as an oncogenic factor in the progression of breast cancer, in that knocking down USP44 inhibited tumor angiogenesis and impaired tumor cell aggressiveness [17, 18]."

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"Consistently, we found that USP44 upregulation effectively inhibited tumor growth in mice (Fig. 2Q, R)."

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"In addition, USP44 overexpression inhibited the growth of the tumors whereas the downregulation of Itch blunted the decline in tumor growth (Fig. 6B–D)."