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"According to the results of the EdU assays, cell proliferation was strongly inhibited by OTUD5 knockdown in HCC cells (P < 0.05, Fig. 2C)."

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"Collectively, these results imply that OTUD5 orchestrates ferroptosis in gastric cancer cells.Moreover, we evaluated the impact of OTUD5 knockout on the cell cycle of gastric cancer cells by an EdU incorporation assay, and the results revealed that OTUD5 depletion decreased the proportion of cells in S phase, indicating impaired cell proliferation (Figure 3M,N)."

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"Consistently, overexpression of OTUD5 promoted the proliferation, while OTUD5 depletion suppressed the proliferation of gastric cancer cells (Figure 3O,P)."

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"These findings demonstrate that both OTUD5 knockdown and nutlin‐3a treatment can induce ferroptosis and suppress cell proliferation."

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"We treated control and OTUD5‐KO cells with nutlin‐3a and observed that knockout of OTUD5, in combination with nutlin‐3a treatment, led to a reduction in protein levels of OTUD5 and GPX4 (Figure 5A,B), thereby triggering ferroptosis in cancer cells and consequently inhibiting cell proliferation (Figure 5C,D)."

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"Taken together, these findings indicate that OTUD5 promotes HCC cell proliferation via SLC38A1."

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"Thus, the above evidence seems to support the high expression of OTUD5 in HCC, especially in HBV-related HCC.In our study, overexpression of OTUD5 promoted the proliferation of HCC cells, while OTUD5 knockdown inhibited cell proliferation, which was also confirmed in vivo."

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"SLC38A1 silencing prominently attenuated the OTUD5-induced increase in HCC cell proliferation."

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"OTUD5 promotes the proliferation of HCC cells."

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"Importantly, SLC38A1 knockdown significantly attenuated the OTUD5-induced increase in proliferation of HCC cells."