IndraLab

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UCHL3 activates AHR. 12 / 12
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"Taken together, experimental data from the present study delineated that LINC00665 acted as a miR-582-5p sponge to up-regulate UCHL3 levels, and enhanced the stability of AhR protein, thereby reducing the radiosensitivity and promoting the immune escape in NSCLC cells."

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"Generally, these findings indicated that as a DUB of AhR, UCHL3 increases AhR protein stabilization in a DUB activity-dependent manner."

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"Collectively, these findings indicate that inhibition of UCHL3 may effectively eliminate lung cancer stem cell properties by promoting AhR destabilization."

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"UCHL3 potentiates the resistance of NSCLC cells to radiotherapy by stabilizing AhR protein."

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"Together, these results indicated that UCHL3 enhanced the radioresistance of NSCLC cells by stabilizing AhR protein."

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"UCHL3 increased AhR stability and the binding of AhR to the promoter regions of the "stemness" genes ATP-binding cassette subfamily G member 2 (ABCG2), KLF4, and c-Myc."

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"In this paper, we found a new mechanism of AhR regulation and functional mechanism by which UCHL3 promotes lung cancer progression and stemness."

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"In summary, our experiments indicate that UCHL3 is a specific DUB for AhR and that UCHL3 elevates AhR protein stabilization through deubiquitination.We further detected mRNA levels in 35 paired ADC and SCC lung cancer and corresponding paracancerous normal tissues (Supplementary Fig. S4b, c) and noted no difference between histologic subtypes."

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"As a deubiquitination, UCHL3 has been suggested to maintain cancer stem-like properties and accelerate tumor cell growth by stabilizing AhR protein [11]."

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"In summary, our findings revealed that AhR plays a critical role in maintaining the stem-like properties of cells overexpressing UCHL3, confirming that UCHL3 promotes tumor stem-like properties through stabilizing AhR."

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"UCHL3 increases AhR protein stability in a DUB activity-dependent manner."

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"Collectively, our in vivo data suggested that LINC00665 augmented the immune escape of NSCLC cells through promoting UCHL3-mediated stabilization of AhR protein via the miR-582-5p/UCHL3 regulatory axis."