The Roles of JNK1 and Stat3 in the Response of Head and Neck Cancer Cell Lines to Combined Treatment with All t<i>rans</i>‐retinoic Acid and 5‐Fluorouracil

Masuda, Munetaka; Toh, Satoshi; Koike, Koji; Kuratomi, Yuichiro; Suzui, Masumi; Deguchi, Atsuko; Komiyama, S.; Weinstein, I. Bernard

doi:10.1111/j.1349-7006.2002.tb02176.x

Cited by 41 publications

(34 citation statements)

References 46 publications

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“…28 STAT3 activation has been shown to be crucial for tumor growth in animal models of SCCHN, and inhibition of STAT3 activity is an interesting therapeutic option. [32][33][34] However, there are no data that suggest usefulness of STAT3 as a marker to predict response to conventional chemotherapy in SCCHN patients.…”

Section: Discussionmentioning

confidence: 99%

STAT1 activation in squamous cell cancer of the oral cavity

Laimer¹,

Spizzo²,

Obrist³

et al. 2007

Cancer

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Thermal degradation of poly(dimethylsilylene) homopolymer (PDMS) and poly(tetramethyldisilylene‐co‐styrene) copolymer (PTMDSS) was investigated by pyrolysis‐gas chromatography and thermogravimetry (TG). PDMS decomposes by depolymerization, producing linear and cyclic oligomeric products, whereas PTMDSS decomposes by random degradation along the chain resulting in each monomeric product and various other combination products. The homopolymer was found to be much less stable than the copolymer. The decomposition mechanisms leading to the formation of various products are shown. The kinetic parameters of thermal degradation were evaluated by different integral methods using TG data. The activation energies of decomposition (E) for the homopolymer and the copolymer are found to be 122 and 181 kJ/mol, respectively, and the corresponding values of order of reaction are 1 and 1.5. The observed difference in the thermal stability and the values of the kinetic parameters for decomposition of these polymers are explained in relation with the mechanism of decomposition. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci, 2006

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Section: Discussionmentioning

confidence: 99%

STAT1 activation in squamous cell cancer of the oral cavity

Laimer¹,

Spizzo²,

Obrist³

et al. 2007

Cancer

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“…Since JNK is necessary for the induction of apoptosis by Taxotere, we investigated whether ATRA also had an effect on this pathway. Others have demonstrated that JNK is activated by ATRA (Wang et al, 2001;Masuda et al, 2002) and other retinoids Zhang et al, 1999). The activation of JNK by retinoids is cell type and system specific, however, since retinoids can also inhibit JNK activation (Lee et al, 1999;Moreno-Manzano et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…JNK is activated by cell stress, including ultraviolet light and hydrogen peroxide (Abate et al, 1990;Chen et al, 1996;Butterfield et al, 1997), and has been implicated in the induction of programmed cell death (Cosulich and Clarke, 1996). Taxotere can activate JNK (Wang et al, 1998), and so can retinoids Zhang et al, 1999;Wang et al, 2001;Masuda et al, 2002). In this study, we investigated the capacity of ATRA to potentiate the cytotoxicity of Taxotere in several breast and prostate cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

All-trans retinoic acid potentiates Taxotere-induced cell death mediated by Jun N-terminal kinase in breast cancer cells

Wang¹,

Wieder²

2004

Oncogene

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Taxotere is a cytotoxin effective in treating breast and prostate cancer. It stabilizes microtubules and causes catastrophic cell cycle arrest in G2/M. Taxanes also initiate apoptosis by activating signal pathways, such as the jun N-terminal kinase (JNK) pathway. Strategies aimed at potentiating cell death signaling may improve their efficacy while lessening the potential side effects. We reported that all-trans retinoic acid (ATRA) potentiated taxane-mediated cell death. Here we investigated whether ATRA potentiates cell death signaling through the JNK pathway. Activation of JNK by Taxotere 0.01, 0.1 and 1.0 lm was observed at 24 h in adherent cells and increased at 48 h. Taxotere 0.001 lm-induced JNK activation started after 48 h and increased at 72 h. The timing and intensity of PARP cleavage was similar to that of JNK activation. JNK activation and PARP cleavage induced by 30 nm Taxotere at 48 h were reversed by curcumin, PD169316 and SP600125, JNK inhibitors in order of progressive specificity. None of these inhibitors had an effect on p38 or ERK phosphorylation. All three inhibitors reversed Taxotere-induced phosphorylation of Bcl-2. ATRA induced JNK activation at 24, 48 and 72 h. Incubating cells with ATRA 0.01 lm for 3 days prior to Taxotere treatment potentiated Taxotere-induced JNK activation 24 and 48 h later, an effect sustained for 72 h. Cytotoxicities from 3-day ATRA 0.01 lm incubations were synergistic with subsequent 1-h Taxotere 0.01, 0.1 and 1.0 lm incubations in breast cancer cell lines MCF-7 and MDA-MB-231 and in prostate cancer cell lines LNCaP and PC-3, and additive in breast cancer cell line SK-Br-3. These data demonstrate the potentiation of Taxotere-induced cell death by ATRA pretreatment in breast and prostate cancer cells, and support a mechanism through accentuated and sustained JNK activation.

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“…12,29 Studies in renal, squamous, and gastric cancers have found that the expression of pSTAT3 in these tumors was associated with an inferior prognosis. 30,31 In lymphoma, it has been reported that ABC DLBCL lines are positive for pSTAT3, whereas GCB DLCBL lines are pSTAT3 negative. 14,15 To date, there have been no studies relating pSTAT3 to survival parameters in DLBCL.…”

Section: Discussionmentioning

confidence: 99%

Expression of Myc, but not pSTAT3, is an adverse prognostic factor for diffuse large B-cell lymphoma treated with epratuzumab/R-CHOP

Gupta¹,

Maurer²,

Wellik³

et al. 2012

Blood

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35% of cases were pSTAT3-positive, and pSTAT3 positivity was more frequent in the non-GCB (P ‫؍‬ .06) type but did not correlate with event-free survival (EFS). Myc expression was observed in 50% of cases and was more frequent in non-GCB type (P ‫؍‬ .07). Myc-positive cases had inferior EFS in all patients, including the GCB and pSTAT3-positive cases, were more likely to express Myc (P ‫؍‬ .06). Myc translocations involving the major breakpoint regions were found in 10% (3 of 29) of cases, and all 3 cases were GCB and had an inferior EFS (P ‫؍‬ .09). pSTAT3, but not Myc expression, was correlated with elevated pretreatment serum cytokines, such as IL-10 (P ‫؍‬ .05), G-CSF (P ‫؍‬ .03), and TNF-␣ (P ‫؍‬ .04). pSTAT3 IHC in DLBCL tumors has the potential to identify patients for STAT3 pathway-directed therapy; Myc IHC is a potential marker for inferior EFS in GCB patients. (Blood. 2012; 120(22):4400-4406) IntroductionThe most significant advance in the treatment of diffuse large B-cell lymphoma (DLBCL) over the past 15 years has been the addition of rituximab to standard CHOP chemotherapy (R-CHOP). [1][2][3] We recently demonstrated in a phase 2 study (N0489; www.clinicaltrials.gov, #NCT00301821) that the anti-CD22 monoclonal antibody epratuzumab can be successfully added to R-CHOP (ER-CHOP) without additional toxicity and with potentially improved survival parameters. 4 Despite these advances, 30%-40% of patients still relapse and die of disease. Current pathology practice classifies DLBCL into at least 3 distinct subtypes: germinal center B cell-like (GCB), activated B cell-like (ABC), and primary mediastinal B-cell lymphoma by gene expression profiling or immunohistochemistry (IHC). 5,6 These classifications are being evaluated in new DLBCL trials, and there have been some reports suggesting that agents, such as bortezomib and lenalidomide, are more effective in non-GCB type DLBCL. 7,8 To improve outcomes for DLBCL patients, it is necessary to identify additional novel targets within GCB and non-GCB classifications to further stratify patients for prognosis and assist in choosing therapy for the individual patient.Signal transducer and activator of transcription 3 (STAT3) is a latent cytoplasmic transcription factor that resides in the cytoplasm. 9 Phosphorylation of STAT3 (pSTAT3) at its Tyr-705 residue (pSTAT3 Tyr705 ) leads to activation and translocation to the nucleus where pSTAT3 regulates several target genes, such as MYC. 10,11 Constitutively active STATs (particularly STAT3 and STAT5) contribute to the malignant phenotype in both human cancer cell lines and primary tumors. 12,13 Recently, it has been reported that STAT3 is overexpressed in ABC-type DLBCL human cell lines. 14,15 The role of pSTAT3 as a prognostic factor in DLBCL patients treated with R-CHOP-based therapies is unknown.Translocations involving the MYC gene at 8q24 are associated with Burkitt lymphoma. 16 Moreover, MYC translocations have been reported to occur in DLBCL with a frequency of 5%-10%. [17][18][19] Myc protein can be expressed ...

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The Roles of JNK1 and Stat3 in the Response of Head and Neck Cancer Cell Lines to Combined Treatment with All trans‐retinoic Acid and 5‐Fluorouracil

Cited by 41 publications

References 46 publications

STAT1 activation in squamous cell cancer of the oral cavity

STAT1 activation in squamous cell cancer of the oral cavity

All-trans retinoic acid potentiates Taxotere-induced cell death mediated by Jun N-terminal kinase in breast cancer cells

Expression of Myc, but not pSTAT3, is an adverse prognostic factor for diffuse large B-cell lymphoma treated with epratuzumab/R-CHOP

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