IndraLab

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JOSD2 activates Neoplasms. 10 / 10
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"This newly identified catalytic site can serve as a potential target for developing inhibitors against JOSD2 catalytic activity.In attempts to elucidate the underlying mechanisms of tumor-promoting effect of JOSD2, we found that overexpression of JOSD2 removes K6-linked polyubiquitination of LKB1, and the deubiquitination of K6 linkage of LKB1 leads to disruption of LKB1/STRAD/MO25 complex integrity, thus inhibits kinase activity of LKB1 and downstream AMPK signaling pathway, so as to induce cell proliferation."
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"We then further ask whether the tumor-promoting effect of JOSD2 is dependent on its regulatory effect on LKB1."
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"Moreover, patient derived cell (PDC) and patient-derived xenograft (PDX) model were further introduced to validate the YAP/TAZ regulation and tumor-promoting roles of JOSD2 in CCA patients."
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"Taken together, these data confirmed that depletion of JOSD2 significantly arrested the NSCLC cell proliferation in vitro and tumor growth in vivo."
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"In vivo xenograft assays further confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC."
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"In vivo xenograft assays confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC."
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"Nonetheless, in LKB1-null cells, silencing JOSD2 still exhibited a certain inhibitory effect on the proliferation, suggesting that other protein substrates in addition to LKB1, might also be involved in JOSD2-driven NSCLC proliferation and cannot be excluded.To further demonstrate that the tumor-promoting effect of JOSD2 depends on LKB1, LKB1-WT and LKB1-3KR were introduced to LKB-null NCI-H460 cells."
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"More importantly, JOSD2 distinctly accelerated the in vivo tumor growth in NCI-H460 xenografted tumors harboring LKB1-WT, but exerting minimal impact in control and LKB1-3KR groups (Fig. 5h–j)."
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"Taken together, the tumor-promoting effect of JOSD2 is dependent, at least partially, on its regulation on LKB1."
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"Consistently, JOSD2 silence markedly decreased >50% tumor weight (P < 0.01, Fig. 5C)."
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