Comparison of Kinome Profiles of Barrett's Esophagus with Normal Squamous Esophagus and Normal Gastric Cardia

Baal, Jantine W. P. M. van; Diks, Sander H.; Wanders, Ronald J. A.; Rygiel, Agnieszka Magdalena; Milano, Francesca; Joore, Jos; Bergman, Jacques J.G.H.M.; Peppelenbosch, Maikel P.; Krishnadath, Kausilia K.

doi:10.1158/0008-5472.can-06-1370

Cited by 73 publications

(64 citation statements)

References 33 publications

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“…To this end, a peptide array was used, which contains 1,176 different kinase substrate consensus sequences, generating a comprehensive overview of the total complement of cellular kinase activity and thus enabling analysis of celecoxib effects without a priori assumptions as to signaling pathways affected by the compound. The generated data have been extensively validated (24)(25)(26)(27)(28). Our results suggest that celecoxib represses c-Met-dependent signaling, resulting in down-regulation of oncogenic Wnt signaling in CRC.…”

Section: Introductionmentioning

confidence: 66%

Cyclooxygenase-2 Inhibition Inhibits c-Met Kinase Activity and Wnt Activity in Colon Cancer

Tuynman¹,

Vermeulen²,

Boon³

et al. 2008

Cancer Research

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124

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Activity of receptor tyrosine kinases (RTK) in colorectal cancer (CRC) is associated with enhanced tumor growth and a poorer prognosis. In addition, cyclooxygenase-2 (COX-2) expression contributes to tumor growth and invasion. COX-2 inhibitors exhibit important anticarcinogenic potential against CRC, but the molecular mechanism underlying this effect and the relation with RTK signaling remain the subject of intense research effort. Therefore, the rapid effects of COX-2 inhibition in CRC on the complement of all cellular kinases were investigated using a kinase substrate peptide array, Western blotting, transfection, small interfering RNA assays, and CRC cell lines. The resulting alterations in the kinome profile revealed that celecoxib, a selective COX-2 inhibitor, impairs phosphorylation of substrates for the RTKs c-Met and insulinlike growth factor receptor, resulting in decreased downstream signaling. The decrease in c-Met activation is accompanied with an increase in glycogen synthase kinase 3B kinase activity together with a rapid increase in phosphorylation of B-catenin. In agreement, a significant reduction of B-catenin-T-cell factor-dependent transcription is observed both with celecoxib and selective inhibition of c-Met phosphorylation by small molecules. Hence, corepression of c-Met-related and Bcatenin-related oncogenic signal transduction seems a major effector of celecoxib in CRC, which provides a rationale to use c-Met inhibitors and celecoxib analogous to target c-Met and Wnt signaling in a therapeutic setting for patients with CRC.

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Section: Introductionmentioning

confidence: 66%

Cyclooxygenase-2 Inhibition Inhibits c-Met Kinase Activity and Wnt Activity in Colon Cancer

Tuynman¹,

Vermeulen²,

Boon³

et al. 2008

Cancer Research

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124

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“…The PepChipH kinome array (Pepscan Systems, Lelystad, The Netherlands) consisting of 1024 peptides with specific phosphorylation sites was used to evaluate the kinome after TRAIL treatment in NSCLC cells, similarly as described previously (Parikh et al, 2009;van Baal et al, 2006). Lysates generated from H460 and A549 cells treated with or without TRAIL (15 min) were analyzed in the assays.…”

Section: Kinome Profiling Arraysmentioning

confidence: 99%

“…A value of 1.96 was taken, which yields a P-value of at least 0.05. A list of peptides was generated by ranking the spots and curve-fitting analysis, resulting in an 'on' or 'off' call for each peptide used to create provisional signal transduction schemes as described earlier [van Baal et al, 2006].…”

Section: Pepchiph Data Analysismentioning

confidence: 99%

Kinome profiling of non-canonical TRAIL signaling reveals RIP1-Src-STAT3 dependent invasion in resistant non-small cell lung cancer cells

Azijli

Yuvaraj

Peppelenbosch

et al. 2012

Journal of Cell Science

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SummaryTumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) triggers apoptosis selectively in tumor cells through interaction with TRAIL-R1/DR4 or TRAIL-R2/DR5 and this process is considered a promising avenue for cancer treatment. TRAIL resistance, however, is frequently encountered and hampers anti-cancer activity. Here we show that whereas H460 non-small cell lung cancer (NSCLC) cells display canonical TRAIL-dependent apoptosis, A549 and SW1573 NSCLC cells are TRAIL resistant and display protumorigenic activity, in particular invasion, following TRAIL treatment. We exploit this situation to contrast TRAIL effects on the kinome of apoptosis-sensitive cells to that of NSCLC cells in which non-canonical effects predominate, employing peptide arrays displaying 1024 different kinase pseudosubstrates more or less comprehensively covering the human kinome. We observed that failure of a therapeutic response to TRAIL coincides with the activation of a non-canonical TRAIL-induced signaling pathway involving, amongst others, Src, STAT3, FAK, ERK and Akt. The use of selective TRAIL variants against TRAIL-R1 or TRAIL-R2 subsequently showed that this non-canonical migration and invasion is mediated through TRAIL-R2. Short-hairpin-mediated silencing of RIP1 kinase prevented TRAIL-induced Src and STAT3 phosphorylation and reduced TRAIL-induced migration and invasion of A549 cells. Inhibition of Src or STAT3 by shRNA or chemical inhibitors including dasatinib and 5,15-diphenylporphyrin blocked TRAIL-induced invasion. FAK, AKT and ERK were activated in a RIP1-independent way and inhibition of AKT sensitized A549 cells to TRAILinduced apoptosis. We thus identified RIP1-dependent and -independent non-canonical TRAIL kinase cascades in which Src and AKT are instrumental and could be exploited as co-targets in TRAIL therapy for NSCLC.

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“…Data were exported to a spreadsheet for further analysis. The raw data were normalized to the 90th percentile, as described previously (15)(16)(17)(18). From this data, the heat map in Figure 1 was constructed in R 2.12.0 (R Foundation for Statistical Computing, Vienna, Austria) using the heatmap.2 function of the gplots library, making use of the hclust function set using complete-linkage.…”

Section: Discussionmentioning

confidence: 99%

Kinase Activity Profiling of Gram-Negative Pneumonia

Hoogendijk

Diks

Peppelenbosch

et al. 2011

Mol Med

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Pneumonia is a severe disease with high morbidity and mortality. A major causative pathogen is the Gram-negative bacterium Klebsiella (K.) pneumoniae. Kinases play an integral role in the transduction of intracellular signaling cascades and regulate a diverse array of biological processes essential to immune cells. The current study explored signal transduction events during murine Gram-negative pneumonia using a systems biology approach. Kinase activity arrays enable the analysis of 1,024 consensus sequences of protein kinase substrates. Using a kinase activity array on whole lung lysates, cellular kinase activities were determined in a mouse model of K. pneumoniae pneumonia. Notable kinase activities also were validated with phospho-specific Western blots. On the basis of the profiling data, mitogen-activated protein kinase (MAPK) signaling via p42 mitogen-activated protein kinase (p42) and p38 mitogen-activated protein kinase (p38) and transforming growth factor β (TGFβ) activity were reduced during infection, whereas v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian) (SRC) activity generally was enhanced. AKT signaling was represented in both metabolic and inflammatory (mitogen-activated protein kinase kinase 2 [MKK], apoptosis signal-regulating kinase/mitogen-activated protein kinase kinase kinase 5 [ASK] and v-raf murine sarcoma viral oncogene homolog B1 [b-RAF]) context. This study reaffirms the importance of classic inflammation pathways, such as MAPK and TGFβ signaling and reveals less known involvement of glycogen synthase kinase 3β (GSK-3β), AKT and SRC signaling cassettes in pneumonia.

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Comparison of Kinome Profiles of Barrett's Esophagus with Normal Squamous Esophagus and Normal Gastric Cardia

Cited by 73 publications

References 33 publications

Cyclooxygenase-2 Inhibition Inhibits c-Met Kinase Activity and Wnt Activity in Colon Cancer

Cyclooxygenase-2 Inhibition Inhibits c-Met Kinase Activity and Wnt Activity in Colon Cancer

Kinome profiling of non-canonical TRAIL signaling reveals RIP1-Src-STAT3 dependent invasion in resistant non-small cell lung cancer cells

Kinase Activity Profiling of Gram-Negative Pneumonia

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