IndraLab

Statements

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"JOSD2 has been shown to promote non-small cell lung cancer (NSCLC) cell proliferation by stabilizing metabolic enzymes aldolase A and phosphofructokinase-1, suggesting that JOSD2 is a positive regulator of glucose metabolism [4]."
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"The results showed that JOSD2 overexpression significantly promoted the proliferation (P < 0.0001), drug resistance (P < 0.0001), migration (P < 0.01), and invasion (P < 0.001) capability of KYSE30 cells (Figure 5C-E)."
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"JOSD2 promotes ESCC cell proliferation and drug resistance in vivo."
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"In vivo xenograft assays confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC."
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"The depletion of JOSD2 significantly impaired the proliferation of CCA cells."
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"JOSD2 promotes cell proliferation, migration, and drug resistance in ESCC."
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"As expected, JOSD2 overexpression significantly promoted cell proliferation of LKB-WT NSCLC cells NCI-H1299 and PC-9, with no appreciable change in LKB-null cells A549 and NCI-H460 (Fig. 5a–d)."
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"Correspondingly, JOSD2 depletion significantly inhibited the cell proliferation in these NSCLC cells harboring LKB-WT (Fig. 1e), whereas imposed a weaker effect on LKB-null cells A549 cells at least under our experimental condition (Supplementary Fig. S7d, e)."
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"We found that JOSD2 depletion by RNA interference robustly inhibited the proliferation of both PDC cells in vitro (Fig. 6b), accompanied with the activation of p-LKB (Supplementary Fig. S8a)."
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"JOSD2 deficiency inhibits tumor cell proliferation by reducing glycolysis, and its mRNA expression is related to the worst prognosis in NSCLC (Krassikova et al., 2021)."
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"We first examined the effects of JOSD2 knockdown on KRAS-mutant CRC cell growth and found depletion of JOSD2 dramatically inhibited the proliferation and colony formation of KRAS-mutant CRC cells SW480, SW620, and HCT-116 in vitro (Supplementary Fig. 3a–d)."
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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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"Subsequent analyses revealed that JOSD2 significantly enhanced the proliferation, migration, and drug resistance of ESCC cells."
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"For cancer types that are highly reliant on glycolysis for their energy supply, increased JOSD2 expression significantly promoted cell proliferation and growth."
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"These results collectively indicate that YAP/TAZ have critical roles in CCA proliferation and JOSD2 is a potential oncogenic DUB in YAP/TAZ-related CCA.3.2 JOSD2 promotes CCA cells proliferation and stabilizes YAP/TAZ proteins."
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"Moreover, depletion of JOSD2 notably inhibited KRAS-mutant NSCLC cell proliferation, which is consistent with the results observed in KRAS-mutant CRC."
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"JOSD2 knockdown inhibited ESCC cell activity, including proliferation and colony-forming ability."
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"In vivo xenograft assays further confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC."
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"JOSD2 enhances ESCC cell proliferation, drug resistance, and migration in vitro."
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