mir141 and mir200a act on ovarian tumorigenesis by controlling oxidative stress response although there is evidence that redox regulation has an essential role in malignancies its impact on tumor prognosis remains unclear here we show crosstalk between oxidative stress and the mir200 family of micrornas that affects tumorigenesis and chemosensitivity mir141 and mir200a target p38 and modulate the oxidative stress response enhanced expression of these micrornas mimics p38 deficiency and increases tumor growth in mouse models but it also improves the response to chemotherapeutic agents highgrade human ovarian adenocarcinomas that accumulate mir200a have low concentrations of p38 and an associated oxidative stress signature the mir200adependent stress signature correlates with improved survival of patients in response to treatment therefore the role of mir200a in stress could be a predictive marker for clinical outcome in ovarian cancer in addition although oxidative stress promotes tumor growth it also sensitizes tumors to treatment which could account for the limited success of antioxidants in clinical trials