STAT3 activation is required for interleukin-6 induced transformation in tumor-promotion sensitive mouse skin epithelial cells

Yu, Cheng‐Rong; Wang, Lihua; Khaletskiy, Alexander; Farrar, William L.; Larner, Andrew C.; Colburn, Nancy H.; Li, Jian Jian

doi:10.1038/sj.onc.1205499

Cited by 39 publications

(27 citation statements)

References 58 publications

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“…However, p21 showed little response to anticancer agent-induced stress in some tumor cells. Loss of p21 results in an induction of apoptosis, but no difference was found in the clonogenic survival (47,48), in IR-induced S-phase checkpoint (41), or in DNA repair responses to UV radiation (21). We report here that, although p53 and p21 were activated in IR-derived MCFϩFIR cells, no difference was detected in p21 protein and nuclear translocation in control and MCFϩFIR cells after IR.…”

Section: Discussionmentioning

confidence: 62%

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p53 Activation in Chronic Radiation-Treated Breast Cancer Cells

Xia

Paik

2004

Cancer Research

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Mammalian cells chronically exposed to ionizing radiation (IR) induce stress response with a tolerance to the subsequent cytotoxicity of IR. Although p53 is well documented in IR response, the signaling network causing p53 activation in chronic IR remains to be identified. Using breast carcinoma MCF؉FIR cells that showed a transient radioresistance after exposure chronically to fractionated IR (FIR), the present study shows that the basal DNA binding and transcriptional activity of p53 was elevated by FIR. p53-controlled luciferase activity was strikingly induced (ϳ7.9-fold) with little enhancement of p53/DNA binding activity (

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Section: Discussionmentioning

confidence: 62%

“…Cytoplasmic and nuclear proteins were extracted as described previously (41). Briefly, sham-FIR control MCF-7 and MCFϩFIR cells were exposed to a single dose of 5 Gy of radiation, collected with trypsin, and washed three times with PBS.…”

Section: Introductionmentioning

confidence: 99%

p53 Activation in Chronic Radiation-Treated Breast Cancer Cells

Xia

Paik

2004

Cancer Research

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“…5). Given that the capacity of anchorageindependent growth of Cl41 cells in soft agar indicates the tumorigenicity of the cells in nude mouse (Colburn et al, 1988;Huang et al, 1998;Li et al, 1997;Yu et al, 2002), COX-2 induction at least partially contributed to TNF-␣-induced transformation of Cl41 cells. In addition, Dhar et al reported that specific and non-specific iNOS inhibitors significantly reduced TNF-␣-induced NO production in Cl41 cells, whereas both of them enhanced the TNF-␣-induced cell transformation (Dhar et al, 2003), which suggests that iNOS may not play an essential role in TNF-␣-induced cell transformation in Cl41 cells (Dhar et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The JB6 P + Cl41 cell is a transformation-susceptible cell line, and has been widely used as a model for anchorage-independent cell growth to indicate cell transformation based on the fact that cells growing in soft agar can form tumors in nude mice (Colburn et al, 1988;Huang et al, 1998;Li et al, 1997;Yu et al, 2002). We demonstrated that induction of COX-2, but not iNOS by TNF-␣ was abolished by knockdown of NFAT3 expression by its specific siRNA, and TNF-␣-induced anchorageindependent growth was greatly inhibited by knockdown of NFAT3 or COX-2.…”

Section: Introductionmentioning

confidence: 99%

NFAT3 is specifically required for TNF-α-induced cyclooxygenase-2 (COX-2) expression and transformation of Cl41 cells

Yan

Ouyang

et al. 2006

Journal of Cell Science

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“…A recent study showed that STAT3 activation is required for interleukin-6-induced transformation in tumor promotion-sensitive mouse skin epithelial cells (43). Another report showed that transformation of normal fibroblasts cells with E1A ϩ Ha-Ras oncogenes causes a constitutive activation of STAT1 and STAT3 transcription factors (44).…”

Section: P38 Map Kinase Regulates Cell Transformation Induced By Egfdmentioning

confidence: 99%

p38 Mitogen-activated Protein Kinase Regulation of JB6 Cl41 Cell Transformation Promoted by Epidermal Growth Factor

Cho

et al. 2003

Journal of Biological Chemistry

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The relationship between cell transformation and p38 MAP kinase, a major mitogen-activated protein (MAP) kinase pathway converting signals of various extracellular stimuli into expression of specific target genes through activation of transcription factors, still remains unclear. The aim of the present study was to investigate the role of the p38 MAP kinase pathway in epidermal growth factor (EGF)-induced cell transformation in JB6 cells. Our data show that a dominant negative mutant of p38 MAP (DN-p38) kinase inhibits EGF-promoted JB6 Cl41 cell transformation and that SB202190, an inhibitor of p38 MAP kinase, also inhibits JB6 Cl41 cell transformation in a dose-dependent manner. Moreover, our results show that DN-p38 MAP kinase inhibits the phosphorylation of EGF-stimulated activating transcription factor-2 (ATF-2) and signal transducer and activator of transcription 1 (STAT1). Additionally, DN-p38 MAP kinase inhibits EGF-induced phosphorylation of c-Myc The mitogen-activated protein kinases (MAPKs), 1 including p38 kinase, c-Jun NH 2 -terminal kinases (JNKs), extracellular signal-regulated kinases (ERKs), and signal transduction cascades, are vital mediators of many cellular functions such as growth, development, proliferation, differentiation, malignant transformation, inflammation, and apoptosis (1-3). p38 MAP kinase is activated by cellular stresses including inflammatory cytokines, ultraviolet light, and growth factors, and the activated p38 MAP kinase has been shown to phosphorylate several transcription factors including ATF-2, STAT1, the Max/ Myc complex, and myocyte enhancer factor 2 (MEF2) (1, 4 -6). On the other hand, ERKs are predominantly activated by mitogenic stimuli, including mitogens and growth factors, and activated ERKs are involved in cell differentiation and development (2, 3). Although one major function of the p38 kinase and JNKs pathways is regulation of inflammation and apoptosis, in many cases the biological consequences of p38 kinase and JNK activation overlap with those of ERKs in mediation of cell growth and differentiation (2, 3, 6, 7).Previously, we studied ERKs regulation of epidermal growth factor (EGF)-induced cell transformation in promotion sensitive (P ϩ ) derivatives of the mouse epidermal JB6 cell line (8). Results showed that inhibition of ERKs appeared to be an important contributor to the tumor promotion-resistant phenotype in JB6 cells. A recent study showed that the p38 kinase and JNKs pathways cooperate to transactivate the vitamin D receptor through the c-Jun/activator protein-1 (AP-1) (9). This result indicates that a connection exists between p38 MAP kinase and AP-1. But AP-1 activation is involved in JB6 cell transformation promoted by EGF and the phorbol ester 12-Otetradecanoyl-phorbol-13-acetate (TPA) (10, 11). AP-1 is a dimeric complex consisting of proteins encoded by the jun and fos gene families, and the AP-1 binding region in these genes is referred to as the TPA response element (TRE). AP-1 induces the transcription of genes that are related to cell prol...

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STAT3 activation is required for interleukin-6 induced transformation in tumor-promotion sensitive mouse skin epithelial cells

Cited by 39 publications

References 58 publications

p53 Activation in Chronic Radiation-Treated Breast Cancer Cells

p53 Activation in Chronic Radiation-Treated Breast Cancer Cells

NFAT3 is specifically required for TNF-α-induced cyclooxygenase-2 (COX-2) expression and transformation of Cl41 cells

p38 Mitogen-activated Protein Kinase Regulation of JB6 Cl41 Cell Transformation Promoted by Epidermal Growth Factor

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