Activation of the Human p27Kip1 Promoter by IFNα 2b

Single-stranded RNA viruses inactivate the transcriptional activity of p53 but induce NOXA-dependent apoptosis via post-translational modifications of IRF-1, IRF-3 and CREB

“…It is well established that IRF-1 plays an important role in growth arrest due in part to the ability of IRF-1 to modulate the transcription of cytostastic genes such as P21 or P27(kip1) (Tanaka et al, 1996;Moro et al, 2000) or proapoptotic genes such as CASPASE-7, -8 and -1 and FAS ligand (Chow et al, 2000;Sanceau et al, 2000;Ruiz-Ruiz et al, 2004). The results of the present study show that NOXA should be added to the list of the proapoptotic genes upregulated during growth arrest and attest to the central role played by IRF-1 in the induction of apoptotis.…”

The Potentiation of Estrogen on Insulin-like Growth Factor I Action in MCF-7 Human Breast Cancer Cells Includes Cell Cycle Components

“…It is thought that this regulation is primarily at the post-transcriptional level. However, some exceptions have been found in primary cultures of thymocytes (41), myeloid leukemic cell lines (42), and H82 cells (43) in which cAMP, vitamin D 3 , and interferon (␣2b) regulate p27 mRNA levels. In this report, we demonstrate that E2, but not IGF-1, inhibits a human p27 promoter-driven luciferase reporter gene when transiently transfected into MCF-7 cells.…”

Antiestrogen resistance in breast cancer and the role of estrogen receptor signaling

“…While initially identified as an interferon-induced gene, IRF-1 has now been implicated in regulating several critical cellular functions and is a putative tumor suppressor in some cancers (Tanaka et al, 1994a, b;Yim et al, 1997). IRF-1's tumor suppressor activities may be related to its ability to signal to apoptosis (Tanaka et al, 1994a), which can occur in a p53-dependent or -independent manner (Tamura et al, 1995;Tanaka et al, 1996), with or without induction of p21 waf1/cip1 (Tanaka et al, 1996) or p27 kip1 (Moro et al, 2000), and through caspase-1 (Tamura et al, 1995), -7 (Sanceau et al, 2000 -8, (Suk et al, 2001), and/or Fas-ligand (Chow et al, 2000). Potentially related to these activities is the ability of SAPK p38, which is involved in signaling to apoptosis in response to stress, to activate IRF-1/interferon-stimulated reponse element binding (Varley and Dickson, 1999).…”