The Carcinogenic Effect of UVA Irradiation

Staberg, B; Wulf, Hans Christian; Klemp, P; Poulsen, Thomas; Brodthagen, H

doi:10.1111/1523-1747.ep12522855

Cited by 161 publications

(69 citation statements)

References 7 publications

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“…PKCa was used as control for the loaded sample protein Role of Erks in UV-induced AP-1 transactivation C Huang et al Forbes et al, 1976). Experimentally, UV irradiation acts both as a tumor initiator and a tumor promoter in animal models (Staberg et al, 1983;Strickland, 1986). Previous studies demonstrate that induced AP-1 activity is required for tumor promotion (Dong et al, 1995a,b;Huang et al, 1996cHuang et al, , 1998.…”

Section: Discussionmentioning

confidence: 99%

The extracellular-signal-regulated protein kinases (Erks) are required for UV-induced AP-1 activation in JB6 cells

Huang

Dong

1999

Oncogene

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Mitogen activated protein (MAP) kinase belongs to a large family of serine/threonine protein kinases, including extracellular-signal-regulated protein kinases (Erks), P38 kinase and c-Jun N-terminal kinases (JNKs). Although previous work has shown that both Erks and JNKs are activated in cells in response to ultraviolet (UV) irradiation, most studies have focused only on the role of JNKs in UV-induced AP-1 activation. Hence, the role of Erks in UV-induced AP-1 activity is not well de®ned. We here have investigated this issue by using MAP kinase kinase (MEK 1 IntroductionExtensive studies in the last several years have demonstrated that the members of mitogen activated protein kinase (MAPKs) family constitute a superfamily of proteins that include extracellular-signalregulated protein kinases (Erks) and c-Jun N-terminal kinases/stress-activated protein kinases (JNKs/SAPKs) and P38 kinase (Boulton et al., 1990(Boulton et al., , 1991Davis, 1994;Kyriakis et al., 1994;Robbins et al., 1992). These kinases belong to the activated serine/threonine kinases, which are uniquely identi®ed by the ThrXaa-Tyr dual-phosphorylation motif, where Xaa is Glu, Pro and Gly for Erks, JNKs/SAPKs and P38 kinase, respectively (Cobb et al., 1994;Kallunki et al., 1994;Sluss et al., 1994). Phosphorylation of both tyrosine and threonine residues, which are found in the activation segment of the kinase domain, is essential for full kinase activity (Coso et al., 1995;Dalton and Treisman, 1992). The activation of MAPKs may be by translocation to the nucleus, where these kinases phosphorylate target transcription factors such as AP-1 (Coso et al., 1995;Huang et al., 1996a;Rosenberger and Bowden, 1996). It is believed that Erks are strongly activated and play a critical role in transmitting signals initiated by 12-0-tetradecanoylphorbol-13-acetate (TPA) and growth factors such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF) (Cowley et al., 1994;Dalton and Treisman, 1992;L'Allemain et al., 1992;PageÁ s et al., 1993;Robbins et al., 1993;Wan et al., 1996;Xia et al., 1995). Whereas the JNKs/SAPKs and P38 kinases are potently activated by various forms of stress, such as ultraviolet light (UV), heat shock and in¯ammation (Adler et al., 1995(Adler et al., , 1996BuÈ scher et al., 1988; Denhardt, 1996;Ludwig et al., 1996;Minden et al., 1994; SaÂ nchez et al., 1994), the activation of these pathways is not mutually exclusive. For example, heat shock and UV irradiation partially activate the Erk1/Erk2 cascade and EGF partially activates the JNKs/SAPKs pathway (Denhardt, 1996, Minden et al., 1994. Thus, understanding how such speci®city is maintained and the extent and signi®cance of crosstalk between each signaling cascade are very important subjects requiring further investigation.Erks (Erk1 and Erk2) were the ®rst members of the MAPKs superfamily whose cDNA were cloned (Boulton et al., 1990(Boulton et al., , 1991Cobb et al., 1994). The Ras?Raf?MEK?Erks cascade is the signaling cascade that leads to Erks activation. Previous st...

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Section: Discussionmentioning

confidence: 99%

The extracellular-signal-regulated protein kinases (Erks) are required for UV-induced AP-1 activation in JB6 cells

Huang

Dong

1999

Oncogene

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“…Ultraviolet B (UVB) irradiation from sun exposure is thought to be the major cause of human nonmelanoma skin carcinoma (Staberg et al, 1983;Strickland, 1986). One possible mechanism for UVB induced carcinogenesis involves its ability to induce prostaglandin formation.…”

Section: Introductionmentioning

confidence: 99%

Role of cyclic AMP responsive element in the UVB induction of cyclooxygenase-2 transcription in human keratinocytes

et al. 2001

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It has been shown that UVB irradiation induces expression of COX-2 and up-regulation of COX-2 plays a functional role in UVB tumor promotion. In this study, we examined the cis-elements in the human COX-2 promoter that may be responsible for the UVB induction of COX-2. Analyses with the COX-2 promoter region revealed that the cyclic AMP responsive element near the TATA box was essential for both basal and UVB induced COX-2 expression. This was further supported by studies using a dominant negative mutant of CREB, which strongly inhibited the activity of COX-2 promoter. Electrophoretic mobility shift assays indicated that CREB and ATF-1 were the major proteins binding to the COX-2 CRE. CREB and ATF-1 were phosphorylated upon UVB treatment, and SB202190, a p38 MAPK inhibitor, decreased the phosphorylation of CREB/ATF-1 and suppressed COX-2 promoter activity. In contrast, treatment with forskolin, an activator of adenylyl cyclase, led to phosphorylation of CREB and ATF-1 and activation of COX-2 promoter. Finally, enhanced binding of phospho-CREB/ATF-1 to the COX-2 CRE was observed after UVB induction. Thus, one signaling pathway for UVB induction of human COX-2 involves activation of p38, subsequent phosphorylation of CREB/ATF-1, and activation of the COX-2 CRE through enhanced binding of phosphorylated CREB/ ATF-1. Oncogene (2001) 20, 5164 ± 5172.

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“…Experimentally, u.v. irradiation acts as both a tumor initiator and as a tumor promoter in animal models (Staberg et al, 1983;Strickland, 1986). The exposure of mammalian cells to u.v.…”

Section: Introductionmentioning

confidence: 99%

Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

Huang

Dong

1997

Oncogene

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The exposure of mammalian cells to ultraviolet (u.v.) irradiation leads to activation of transcription factors, such as AP-1 and NFkB. It is postulated that the EGF receptor but not protein kinase C (PKC) is the major membrane mediator in UVC-induced signal transduction. We demonstrate here that the antisense oligonucleotides of PKCz and the dominant negative mutant of PKCl/i as well as dominant negative PKCz markedly blocked UVC-induced AP-1 activity. In contrast, UVC-induced AP-1 activity in cells devoid of the EGF receptor (B82), is not signi®cantly di erent from that of the stable transfectants with a kinase-de®cient EGF receptor (B82M721), or wild-type EGF receptor (B82L). This was found at all UVC irradiation doses and time courses studied, while high levels of EGF-induced AP-1 activity were observed in B82L cells but not in B82 cells. This evidence strongly suggests that atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in JB6 and B82 cells.

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The Carcinogenic Effect of UVA Irradiation

Cited by 161 publications

References 7 publications

The extracellular-signal-regulated protein kinases (Erks) are required for UV-induced AP-1 activation in JB6 cells

The extracellular-signal-regulated protein kinases (Erks) are required for UV-induced AP-1 activation in JB6 cells

Role of cyclic AMP responsive element in the UVB induction of cyclooxygenase-2 transcription in human keratinocytes

Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC-induced AP-1 activation in immortal murine cells

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