“…Despite the identified dual functionality of c-FLIPL as a pro- or antiapoptotic factor in normal tissues, c-FLIPL has generally been shown to act as a key negative regulator of apoptosis in human cancer cells [38, 39]. Increased expression of c-FLIP has been detected in many human malignancies, including melanoma, hepatocellular carcinoma [40], nonsmall cell lung carcinoma [40], and endometrial [41], colon [42], and prostate cancer [43–45]. While its overexpression has been associated with cancer progression and/or poor prognosis in BL, HCC, and ovarian, endometrial, colon, and prostate cancer [38, 39, 42, 46], elevated expression of c-FLIP blocks caspase-8 and renders cells resistant to cell receptor-mediated apoptosis [38].…”