IndraLab

Statements


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"Abnormalities of the ubiquitin-proteasome system are key in PAAD pathogenesis, and the ubiquitin-proteasome UCHL5 can promote tumor progression and dry expression depending on involvement of the ELK3 protein (Yang et al., 2022)."

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"Treatment with b-AP15, a UCHL5 and USP14 deubiquitinating activity inhibitor in 19S regulatory subunit, induces tumor regression and prolong the survival period of tumor-loaded mice through down-regulation of COPS5 and its downstream AP-1 and E2F1, and up-regulation of the cell cycle-related proteins p27 and Cyclin E1."

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"On the other hand, UCH37, the deubiquitinase activated by ADRM1, inhibits glioma cell migration and invasion [42], suggesting that ADRM1 inhibition could have a positive or negative effect on tumor progression, depending on the stage of the tumor.The discovery of a new role for HDAC8 and ADRM1 in MGMT regulation expands the possibilities of the development of new therapies to overcome TMZ resistance in GBM, although several questions about the mechanisms remain to be answered."

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"These outcomes demonstrated that UCHL5 can indeed promote tumor development in vivo."

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"The findings demonstrated that the glycolysis route underwent the greatest multiple of change (Fig. 3A), which led us to speculate whether UCHL5 promoted tumor progression by regulating the glycolysis process."

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"B-AP15, an inhibitor of USP14 and UCHL5, can cooperate with imatinib to inhibit the growth of BCR-ABL-WT and BCR-ABL-T315I CML cell lines, CML xenograft tumor, and primary CML cells.154 Meanwhile, in another study, they found that piperlongumine, isolated from piper longum L., can target USP14 and UCHL5 to inhibit the proteasome function of CML cells with or without T315I mutation, weaken the cell viability of CML cell line, induce apoptosis, and inhibit the growth of transplanted tumor."

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"These findings imply that the high expression of UCHL5 in tumors stimulates the expression of genes involved in metabolism, allowing for significant glycolysis and increased energy generation to sustain tumor development."

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"To further confirm the involvement of AKT/mTOR signaling in UCHL5-promoted tumor growth and migration, bladder cancer cells were transfected with pHAGE-puro-UCHL5 and then incubated with LY294002."

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"Upregulation of the TGF signaling pathway is the main mechanism by which UCHL5 modulates malignant tumor progression (151–153)."

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"Additionally, a study on endometrial cancer observed that UCHL5 accelerates tumor growth by activating the Wnt/β-catenin signaling pathway [50]."