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USP24 activates autophagy. 37 / 37
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"Herein we found a positive correlation between targeting USP24-mediated LC3-II signaling and the cytotoxicity of Taxol in drug resistance, implying that targeting USP24-induced autophagy might be important for inhibiting drug resistance during cancer therapy (Fig. 1C)."
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"USP24, another ubiquitinating enzyme, induces autophagy in vivo and in vitro and inhibits drug resistance in cancers acquired by taxol or gefitinib treatment [14]."
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"Overall, targeting USP24 by USP24-i induces autophagy in vitro and in vivo."
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"We also investigated the molecular mechanism of how USP24-mediated autophagy in interphase and mitosis (Fig. 2, Fig. 3 and Supplementary Fig. 2)."
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"Interestingly, autolysosomes were found in mitotic cells (red arrow), indicating that USP24-mediated autophagy occurs not only in interphase but also in mitosis (Fig. 3A)."
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"LC3-II was significantly increased in mitotic A549 cells but not in A549-T24 cells (Fig. 3E(a), Fig. 3E(b) and Fig. 3E(d)), implying that the downregulation of USP24 may induce autophagy to maintain genomic stability in drug-sensitive lung cancer cells but not in drug-resistant lung cancer cells (Fig. 3E)."
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"Targeting USP24 induces autophagy to inhibit drug resistance during lung cancer therapy."
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"What is the role of targeting USP24-mediated autophagy in drug resistance?"
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"Further immunofluorescence detection showed that the addition of the miR-21-5p inhibitor significantly inhibited autophagy, that overexpression of USP24 rescued the influence of the miR-21-5p inhibito[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The data indicated that inhibition of autophagy decreased the cell entry from G2/M (Fig. 4D(b)), and increased chromosome separation defects, micronuclei and segregation defects (Fig. 4E), indicating that autophagic induction during mitosis could maintain genomic stability.Next, the effect of targeting USP24-induced autophagy on chemotherapy- and targeted therapy-induced drug-resistant lung cancer cells was studied (Fig. 4F and Supplementary Fig. 3)."
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"Altogether, these results confirmed that USP24 promotes the autophagy-dependent ferroptosis and increases the sensitivity of HCC cells to sorafenib."
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"Next, we also used gefitinib-induced PC9 drug-resistant cells (PC9-GR) to study the effect of targeting USP24 induced autophagy on inhibiting drug resistance acquired by targeted therapy (Fig. 4F(b), Supplementary Fig. 3A, B)."
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"Gefitinib and USP24-i cocktail treatment significantly induced cell death but abolished this effect by inhibiting autophagy with Baf-A1 or CQ treatment, suggesting that targeting USP24-induced autophagy is essential for the effect of USP24-i on blocking drug resistance acquired by targeted therapy."
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"Our results confirmed that USP24 promotes autophagy-dependent ferroptosis by stabilizing Beclin1 (Fig. 8K)."
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"A glimpse into possible additional cellular strategies in response to intensive treatment regimes in NBT cells comes from findings that USP24 downregulation increases autophagy flux in cells [174]."
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"In summary, targeting USP24-induced autophagy is important for blocking drug resistance acquired by chemotherapy and targeted therapy."
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"In our study, USP24 was found to induce autophagy in HCC."
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"Knockdown of USP24 in cell lines and in human induced-pluripotent stem cells (iPSC) differentiated into dopaminergic neurons resulted in elevated ULK1 protein levels and increased autophagy flux in a manner independent of MTORC1 but dependent on the class III phosphatidylinositol 3-kinase (PtdIns3K) activity."
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"This study revealed that increased autophagy driven by USP24 overexpression was associated with decreased cell viability and increased ferroptosis."
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"Knockdown of USP24 also led to increase in levels of the autophagosome associated lipidated form of LC3 (LC3-II) [30]), confirming increase in autophagy."
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"In addition, the LC3-II levels in the gefitinib/USP24-i-101-treated mice was higher than that in the gefitinib-treated mice, implying that targeting USP24-mediated activation of autophagy may be involved in inhibiting drug resistance in vitro and in vivo (Fig. 7E (d))."
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"Because USP24 is a deubiquitinase, targeting USP24-induced autophagy might be ubiquitin-mediated autophagy."
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"Therefore, overexpression of USP24 induces autophagy along with ferroptosis and reduces sorafenib resistance in HCC [34]."
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"In this study, targeting USP24 induced autophagy was essential for blocking drug resistance acquired by Taxol or gefitinib treatment in vitro and in vivo through a decrease in ABCG2 levels and genomic instability, which can inhibit drug pumping out of cells and clonal selection for drug resistance [3]."
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"USP24 promotes autophagy-dependent ferroptosis in hepatocellular carcinoma by reducing the K48-linked ubiquitination of Beclin1."
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"In this study, targeting USP24-induced autophagy caused cell death, which could be inhibited by bafilomycin A1 or chloroquine treatment."
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"USP24-i-101 targeting of USP24 activates autophagy to inhibit drug resistance acquired during cancer therapy."
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"In this study, targeting USP24-induced autophagy was related to PD-L1 degradation in cancer cells."
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"In this study, we found that targeting USP24 by the specific USP24 inhibitors, USP24-i and its analogues, dramatically activated autophagy in the interphase and mitotic periods of lung cancer cells by inhibiting E2F4 and TRAF6, respectively."
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"USP24 is another modulator of autophagy which may also influence PD progression as it can regulate dopaminergic neurite outgrowth, but the potential as a disease modulator is not evaluated yet."
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"USP24 increases the level of autophagy in HCC cells."
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"Targeting USP24 induces autophagy in vitro and in vivo."
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"To explore the exact mechanism by which USP24 induces autophagy, Co-IP was first carried out to identify the potential substrate of USP24."
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"Blocking lysosomal function with bafilomycin led to significant increase in accumulation of GFP-LC3 positive autophagosomes in USP24 knockdown cells, indicating that USP24 is negatively regulating autophagy flux without affecting lysosomal degradation)."
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"Overall, these evaluations indicated that USP24 increased the level of autophagy in HCC cells."
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"However, Baf-A1 treatment can reverse this effect of USP24-i, indicating that targeting USP24-induced autophagy is involved in the degradation of PD-L1 and ABCG2 (Fig. 6G)."
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"In summary, USP24-i targeting USP24 activates autophagy to promote the degradation of ABCG2 and PD-L1, leading to the inhibition of drug resistance acquired from lung cancer therapy."
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