IndraLab

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"Knockdown of USP35 can inhibit the progression of lung cancer, promote ferroptosis, and increase the sensitivity of lung cancer cells to cisplatin and paclitaxel chemotherapy [142]."

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"Our study uncovers a novel mechanism by which USP35 inhibits ferroptosis in ER+ breast cancer."

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"Knockdown of USP35 promoted cancer cell ferroptosis and inhibited cancer cell growth and metastasis (50)."

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"Despite this, the knockdown of USP35 resulted in increased Lipid ROS levels and inhibited the growth of TNBC cells MDA-MB-231 and SUM159PT (Supplementary Fig. 5B, 1G, 5C), whereas USP35 overexpression partially inhibited ferroptosis induced by Erastin in MDA-MB-231 cells (Supplementary Fig. 9)."

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"Furthermore, USP35 did not interact with BRD4 in TNBC cells (Supplementary Fig. 5D), suggesting that USP35 inhibited ferroptosis independent of the BRD4-SLC7A11 axis in TNBC although BRD4 and SLC7A11 mRNA levels were positively correlated (Supplementary Fig. 7B), which was different from in ER+ breast cancer (Fig. 4)."

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"In lung cancer cells, USP35 interacts directly with FPN1 to maintain its protein stability and prevent iron overload and ferroptosis (Tang Z. et al., 2021)."

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"USP35 combined with transportin (FPN) synergistically stabilized serum ferritin levels and inhibited ferroptosis to delay lung cancer cell growth (124)."

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"In this study, we uncovered that USP35 inhibited ferroptosis of ER+ breast cancer cells."

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"To understand the mechanism by which USP35 inhibits ferroptosis, we examined whether knockdown of USP35 affected the expressions of key ferroptosis regulators in two ER+ breast cancer cell lines."

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"Similarly, the deubiquitinase USP35 stabilized ferroportin and blocked ferroptosis in lung cancer cells [82]."

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"Our results demonstrated that BRD4 inhibition with (+)-JQ-1 treatment significantly inhibited the ER+ breast tumors enhanced by USP35 overexpression, along with decrease of SLC7A11 protein level, and increase of 4-HNE protein levels (Fig. 7), supporting that BRD4 mediated USP35 inhibition of ferroptosis in ER+ breast tumors.Reported studies have shown SLC7A11 expression can be regulated at translational and post-translational levels ."

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"Depletion of USP35 promotes ferroptosis and suppresses lung cancer cell growth and tumor progression [16]."

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"Our data also showed that USP35 inhibits ferroptosis independent of BRD4 in TNBC cells (Supplementary Fig. 5)."

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"Conversely, the deubiquitinating enzyme USP35 interacts with SLC40A1 to maintain the protein stability of iron transporters, preventing the onset of ferroptosis in lung cancer [112]."