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They decreased the expression of CD44, reduced the phosphorylation or expression of EGFR, Met, Akt, and NF-B, completely inhibited EGFR/MET-Akt/NF-B signaling activated by HGF and EGF, and showed a higher inhibition effect on cancer cells when combined with anticancer drugs cytarabine, pyirubicin, vincristine, and methotrexate [48,49,50,51]

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During the ER stress, PERK can be reversible oxidate at Cys216, allowing the interaction with ERO1 narrowing MAM formation and increasing Ca 2+ flux into the mitochondria regulating bioenergetics (Bassot et al
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