IndraLab

Statements



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"Here we show that the remodelling process is regulated by the ubiquitin C-terminal hydrolase UCH-L1 that promotes the invasion of epithelial cells by Listeria monocytogenes and Salmonella enterica."

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"Overexpression of UCHL1 in MKN45 and BGC823 cells promoted cell proliferation, migration, and invasion depending on its de-ubiquitinase activity."

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"Recently, it has been suggested that UCH-L1 promotes cancer cell motility and invasion, which may contribute to its oncogenic role."

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"UCHL1 promotes in vitro clonogenicity, cell proliferation, and invasion."

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"Although our results point to a pivotal role for UCHL1 in stimulating breast cancer extravasation by regulating TGFbeta signaling , we do not preclude that UCHL1 may also promote invasion and metastasis by targeting other signaling proteins ."

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"In non small lung cancer cell line H157, UCHL1 promotes invasion by upstream activation of Akt XREF_BIBR."

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"Through executing loss of function tests, we affirmed that silencing of UCHL1 expression significantly inhibited migration and invasion of lung adenocarcinoma cells in vitro."

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"Recently, UCH-L1 has been found to increase cancer cell migration and invasion by modulating hydrogen peroxide generated by NADPH oxidase 4 (NOX4)."

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"Similarly, CCK-8 assay, scratch assay and transwell assay were applied to demonstrate that overexpression of UCHL1 promoted the proliferation, migration and invasion in SiHa, but when UCHL1 was knockdown in C-33A, the function of UCHL1 displayed the opposite result."

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"This study also showed that UCH-L1 promotes angiogenesis of HUVECs, as well as invasion in cancer cells, by up-regulating ROS by deubiquitination of NOX4, suggesting that UCH-L1 plays a key role in angiogenesis of HUVECS by regulating ROS levels by deubiquitination of NOX4."

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"We propose that C-terminal farnesylation of UCH-L1 facilitates LMP1 loading in exosomes and might promote tumor invasion and metastasis through modulating the cancer microenvironment."

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"UCHL1 is a key promoter of cell invasion and metastasis in small cell lung cancer but not necessarily required for cell viability or proliferation [XREF_BIBR, XREF_BIBR]."

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"These findings indicate that H 2 O 2 levels regulated by UCH-L1 are necessary for cell invasion to occur and demonstrate that UCH-L1 promotes cell invasion by up-regulating H 2 O 2 via deubiquitination of NOX4."

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"In lung adenocarcinoma, UCHL1 promotes tumor migration, invasion, and metastasis by inhibiting apoptosis and has an important impact on the clinical drug treatment of lung adenocarcinoma."

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"Furthermore, Scratch assay and Transwell assay proved that UCHL1 enhanced the migration and invasion of TNBC cells."

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"Our loss of function studies using these pediatric high-grade gliomas cell lines showed that UCHL1 promoted cell growth, invasiveness, and self-renewal characteristics in vitro."

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"51 Finally, UCHL1 and EZR are believed to enhance invasion."

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"These findings demonstrated that UCHL1 promoted cell proliferation, migration, and invasion depending on its de-ubiquitinase activity by activating Akt and Erk1/2, which may account for its higher positive expression rate in liver metastases from gastric cancer."

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"UCHL1 up-regulates beta-catenin signaling and possibly promotes invasion of both Salmonella and Listeria by modulating actin dynamics in the host cell."

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"Thus, these findings demonstrated that UCH-L1 promotes invasion of breast cancer cells and might serve as a potential therapeutic target for treatment of human patients with breast cancers."

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"Recently, UCH-L1 has been known to enhance tumor cell invasion and migration capability via the Akt mediated pathway [53]."

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"The potential role for UCHL1 in promoting breast cancer invasion and metastasis was further supported in a murine breast cancer xenograft model, where UCHL1 overexpressing groups exhibited increased metastasis compared to UCHL1 knockdown groups.To explore the mechanism of action by which UCHL1 promotes breast cancer metastasis, Liu et al. [54] investigated UCHL1 depletion in epithelial–mesenchymal transition (EMT), which has previously been shown to play an important role in breast cancer metastasis [55]."

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"We have further demonstrated that knockdown of UCHL1 decreased cell migration and invasion in a manner that was concomitant with less pseudopod formation in a 3D collagen matrix and significantly redu[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Knocking down NOX4 in B16F10 cells significantly reduced both basal and UCH-L1 enhanced invasiveness of cells, suggesting that both inherent and UCH-L1-enhanced invasiveness of B16F10 cells depend on NOX4."

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"Complementarily, overexpression of UCHL1 enhanced invasion through Matrigel in M10 breast cells."

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"UCH-L1 stimulates prostate cancer cell migration and invasion as well by promoting epithelial-to-mesenchymal transition (EMT) [XREF_BIBR]."

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"Moreover, it has been shown that suppression of UCHL1 inhibits the expression of genes involved in migration in HEK 293 T cells [1] and that UCHL1 enhances invasion in prostate cancer cells through EM[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, cell scratch assay and Transwell assays were performed to explore whether UCHL1 promotes the migration and invasion of TNBC cells."

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"These results demonstrate that UCH-L1 overexpression leads to enhanced H 2 O 2 generation, and that invasion induced by UCH-L1 is reduced by eliminating H 2 O 2, suggesting that UCH-L1 plays a role in the regulation of H 2 O 2 generation."

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"Migration and invasion of SCNEC tumor cells were induced by UCHL1 over-expression and suppressed by UCHL1 down-regulation, as shown by scratch and transwell invasion assays."

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"UCHL1 might promote SCNEC cell migration and invasion by reducing PROX1 ubiquitination ."

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"In lung adenocarcinoma , UCHL1 promotes tumor migration , invasion , and metastasis by inhibiting apoptosis and has an important impact on the clinical drug treatment of lung adenocarcinoma ."

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"In the Transwell and wound healing assays, we found that knockdown of UCHL1 significantly reduced cell migration, motility, and invasiveness."

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"Considering the recently established functional role of extracellular vesicles (ECV) in cancer progression, we suggest that specific inhibition of C-terminal farnesylation of UCH-L1 may reduce invasion and metastasis of EBV associated LMP1 positive metastatic carcinomas."

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"In our previous report, we demonstrated that UCH-L1 promotes prostate cancer cell migration and invasion through EMT induction [11]."