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USP22 activates AKT. 17 / 17
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"USP22 overexpression in gastric cancer cells induces the upregulation of SOS1 and activation of the RAS/ERK and PI3K/AKT pathways."

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"3.5 USP22 activates the AKT and MRP1 pathway depending on SIRT1 in HCC cells."

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"Western blot analysis showed that USP22 overexpression also induced activation of the RAS/ERK and PI3K/AKT pathways in SGC7901 cells and xenograft tumor tissues."

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"Studies have demonstrated that USP22 directly interacts with SIRT1, activating the AKT/GSK-3β/multidrug resistance-associated protein 1 (MRP1) pathway, thereby enhancing 5-Fu efflux and reducing 5-Fu-induced apoptosis in HCC cells [124]."

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"XREF_FIG A, knockdown of USP22 by shRNA inhibited the AKT and MRP1 pathway compared with control shRNA cells and wild-type cells."

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"We found that USP22 promotes multidrug resistance in HCC cells by activating SIRT1/protein kinase B (Akt)/multidrug resistance-associated protein 1 (MRP1) pathway, while inhibition of USP22 and SIRT1 [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Similarly, overexpression of USP22 in BEL/7402 cells activated the AKT and MRP1 pathway."

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"Previous study also showed that USP22 promotes cell cycle progression by positively regulating the PI3K and Akt pathway [XREF_BIBR]."

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"Moreover, SIRT1 deficiency attenuated USP22 induced activation of the AKT and MRP1 pathway in BEL7402 cells, suggesting that USP22 regulated the AKT and MRP1 pathway in a SIRT1 dependent manner."

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"For example, USP22 can stabilize the E2F6 stability and activate Akt pathway in hepatocellular carcinoma (HCC), leading to aggressive progression of HCC (25)."

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"These results suggest that USP22 downregulation inhibits OS cells by suppressing the PI3K and Akt pathway."

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"USP22 directly interacts with SIRT1 and then activates AKT/GSK-3β/MRP1, which, in turn, promotes chemotherapeutic efflux in HCC cells (43)."

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"To investigate whether E2F6 was involved in USP22-promoted AKT activation, we examined p-AKT levels in cells with or without E2F6."

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"It was found that silencing E2F6 remarkably impaired AKT phosphorylation in the steady state ( Fig. 4 C) and effectively counteracted USP22-mediated AKT activation ( Fig. 4 D), indicating that E2F6 st[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Therefore, our data indicate that repression of DUSP1 transcription may underlie the function of USP22-E2F6 in HCC.Next, we investigated whether DUSP1 repression is involved in USP22-mediated AKT acti[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Previous studies have confirmed that USP22 can promote the biological process of NSCLC cells by regulating BMI-1 and AKT signaling pathway [XREF_BIBR]."

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"We observed that USP22 could positively regulate the AKT pathway in a SIRT1 dependent manner."