IndraLab

Statements


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"Together, these results indicate that loss of USP28 decreased MAST1 protein level and suppressed tumor growth upon cisplatin treatment."

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"Moreover, we concentrate on the impacts of USP28 on diverse hallmarks of cancer and discuss whether USP28 can accelerate or inhibit tumor progression."

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"Many studies have demonstrated that USP28 can promote the deubiquitination and stabilization of many oncoproteins, implying that USP28 can stimulate the progression of many tumors."

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"The identification of several DUB inhibitors, including inhibitors of USP28, which regulate various oncogenes (e.g., c-Myc) and USP25, which regulates TRAF (tumor necrosis factor receptor-associated factor) signalling, provide alternative approaches to induce degradation of potential “un-druggable” molecules in cancer.Gerry Melino (University of Cambridge, UK) presented data demonstrating the p53 family protein TAp73, facilitates ubiquitin-dependent degradation of HIF1α, thereby suppressing tumor progression."

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"In SCC tumors, the inhibition of USP28 reduces tumor growth and increases cell death [17]."
| PMC

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"The enzyme has been found to be overexpressed in bladder cancer, glioma, gastric cancer, etc. [12] Besides, multiple studies have shown that the knockdown of USP28 or its inhibition by chemical inhibi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP28 can induce tumor angiogenesis directly and indirectly through the deubiquitination of HIF-1α and c-Myc."

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"The tumor-promoting role of USP28 and relevant investigations are currently dominant; nevertheless, several studies have demonstrated its oncostatic effects."

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"USP28 plays a crucial role in tumor progression, and inhibiting USP28 can suppress the growth of various tumors [1]."

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"Intriguingly, deletion of Usp28 also suppresses intestinal tumor development in the absence of Fbw7, possibly via Fbw7-independent regulation of substrates like Notch, Jun and Myc [102] ."

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"USP28 promotes tumor progression and glycolysis by stabilizing PKM2/Hif1-α in cholangiocarcinoma."

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"Consistently, loss of Usp28 promotes Ras-dependent transformation of mouse fibroblasts via destabilization of Fbw7, indicating that Usp28 may have oncogenic or tumor suppressive functions in different[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Finally, loss of USP28 destabilized MAST1 protein and attenuated tumor growth by sensitizing cells to cisplatin treatment in mouse xenograft model."

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"Acute loss of Usp28 attenuates development of the established tumors and prolongs survival [101] , demonstrating that Usp28 is critical for the maintenance of intestinal tumors and suggesting that inh[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Additionally, loss of USP28 attenuated tumor growth in a mouse xenograft model."

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"Depletion of USP28 reduced tumor size and increased the lifespan of tumor-bearing mice.The chromatin modulator LSD1 controls cellular pluripotency through histone demethylation and is overexpressed in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"USP28 has been reported to promote the proliferation of both tumor and normal cells by stabilizing Claspin [41]."

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"Pard3 deletion led to the up-regulation of USP28, which promoted BC migration and migration via Snail1 stabilization.Given its essential role in tumor metastasis and EMT, Snail1 is considered a key regulator of aggressive phenotypes in tumors."

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"In addition, USP28 knockdown combined with sorafenib inhibited tumor growth and metastasis in tumor xenograft mice model."