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USP36 activates Neoplasms. 9 / 9
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"The xenograft model demonstrated that USP36 depletion significantly reduced ESCC tumor growth in vivo (Figs."
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"Subsequent studies have also found that ALKBH5 and USP36 interact to maintain stem cell properties in glioblastoma and promote tumor progression (Chang et al., 2023[14])."
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"The xenograft model showed that USP36 overexpression significantly promoted ESCC tumor growth in vivo (Figs."
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"These effects are mediated by METTL3 induction of N6-methyladenosine (m A) modifications.Another m A modifier, ALKBH5, is stabilized by the deubiquitinase USP36 in GSCs, stimulating tumor growth and TMZ resistance [193], and this USP36–ALKBH5 relationship may provide another targetable scaffold in GSCs."
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"Furthermore, in vivo xenograft tumor assays revealed that RBM28 silencing exhibited smaller tumors and reversed the promoted tumor growth induced by USP36 expression, as observed in alterations in tumor volume, weight, and Ki67 levels (Fig. 8A, B)."
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"USP36 contributes to the tumor stemness, growth, Oxa-resistance, and metastasis of colon cancer in xenograft models."
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"In the xenograft mouse model, USP36 depletion inhibited tumor growth, and this effect was reversed by YAP overexpression in KYSE150 cells (Figs."
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"Depletion of USP36 significantly reduced the tumor weight , tumor volume and Ki67 staining , indicating that USP36 harbors oncogenic properties ( Figure 3C and D ) ."
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"In summary, overexpression of USP36 in NSCLC accelerated tumor growth through upregulation of KHK-A, which was medicated by stabilizing c-MYC to increase hnRNPH1/H2 expression."
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