P424 Novel Biomarker for Hepatocellular Carcinoma: The Antioxidant Response in the Carcinogenesis

Sánchez‐Rodríguez, Ricardo; Torres-Mena, Julia Esperanza; Quintanar-Jurado, Valeria; Villa‐Treviño, Saúl; Chagoya-Hazas, Victoria; Castillo, Emilio Rojas del; Velasco-Loyden, Gabriela; Pozo‐Yauner, Luis del; Carrillo‐Sánchez, Karol; Pérez‐Carreón, Julio Isael

doi:10.1016/s0168-8278(14)60586-9

Cited by 2 publications

(2 citation statements)

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“…Leukotriene synthetic enzymes, such as MGST3 [28] and GGT1 [29], have been identified as Nrf2 target genes, but GGT1 is also responsive to TNF-A-induced NFkB and Sp1 [30]. Nrf2 is known to control multiple elements in the eicosanoid synthetic pathway, typically via the ARE, as in the case of thromboxane A2 synthase gene activation [31] and the prostaglandin reductase Ptgr1 [32]. Interestingly, early induction of Nrf2 by one of the rhomboid transcription factors has been shown to mediate rapid cutaneous wound healing [33].…”

Section: The Nrf2 System As a Candidate Mediator Of Phytochemical Actionsmentioning

confidence: 99%

RNAseq Analysis of Treatment-dependent Signaling Changes During Inflammation in a Mouse Cutaneous Wound Healing Model.

Laurent

Toma

Seilheimer

et al. 2021

Preprint

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Background: Despite proven therapeutic effects in inflammatory conditions, the specific mechanisms of phytochemical therapies are not well understood. The transcriptome effects of Tr14 (Traumeel), a multicomponent natural product, and diclofenac, a non-selective cyclooxygenase (COX) inhibitor, were compared in a mouse cutaneous wound healing model to identify both known and novel pathways for the anti-inflammatory effect of plant-derived natural products. Methods: Skin samples from abraded mice were analyzed by single-molecule, amplification-free RNAseq transcript profiling at 7 points between 12-192 hours after injury. Immediately after injury, the wounds were treated with either diclofenac, Tr14, or placebo control (n=7 per group/time). RNAseq levels were compared between treatment and control at each time point using a systems biology approach. Results: At early time points (12-36 hours), both control and Tr14-treated wounds showed marked increase in the inducible COX2 enzyme mRNA, while diclofenac-treated wounds did not. Tr14, in contrast, modulated lipoxygenase transcripts, especially ALOX12/15, and phospholipases involved in arachidonate metabolism. Notably, Tr14 modulated a group of cell-type specific markers, including the T cell receptor, that could be explained by an overarching effect on the type of cells that were recruited into the wound tissue. Conclusions: Tr14 and diclofenac had very different effects on the COX/LOX synthetic pathway after cutaneous wounding. Tr14 allowed normal autoinduction of COX2 mRNA, but suppressed mRNA levels for key enzymes in the leukotriene synthetic pathway. Tr14 appeared to have a broad ‘phytocellular’ effect on the wound transcriptome by altering the balance of cell types present in the wound.

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Section: The Nrf2 System As a Candidate Mediator Of Phytochemical Actionsmentioning

confidence: 99%

RNAseq Analysis of Treatment-dependent Signaling Changes During Inflammation in a Mouse Cutaneous Wound Healing Model.

Laurent

Toma

Seilheimer

et al. 2021

Preprint

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“…However, there is evidence in the literature that inhibition of glioma proliferation by non-steroidal anti-inflammatory drugs (NSAIDs) could be mediated partly through upregulation of 15-HPGD [19]. The role of PTGRs in tumor suppression remains inconclusive and is possibly tissue-dependent [20][21][22][23][24]. The prostanoids derived from the activity of COX and their respective synthases are known to contribute to both active inflammation and immune response in the tumor microenvironment [7,25].…”

Section: Introductionmentioning

confidence: 99%

The prostanoid pathway contains potential prognostic markers for glioblastoma

Panagopoulos

Gomes

Almeida

et al. 2018

Prostaglandins & Other Lipid Mediators

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Prostanoids derived from the activity of cyclooxygenases and their respective synthases contribute to both active inflammation and immune response in the tumor microenvironment. Their synthesis, deactivation and role in glioma biology have not yet been fully explored and require further study. Using quantitative real time PCR, gas chromatography/ electron impact mass spectrometry and liquid chromatography/ electrospray ionization tandem mass spectrometry, we have further characterized the prostanoid pathway in grade IV glioblastoma (GBM). We observed significant correlations between high mRNA expression levels and poor patient survival for microsomal PGE synthase 1 (mPGES1) and prostaglandin reductase 1 (PTGR1). Conversely, high mRNA expression levels for 15-hydroxyprostaglandin dehydrogenase (15-HPGD) were correlated with better patient survival. GBMs had a higher quantity of the prostanoid precursor, arachidonic acid, versus grade II/III tumors and in GBMs a significant positive correlation was found between arachidonic acid and PGE content. GBMs also had higher concentrations of TXB, PGD, PGE and PGF versus grade II/III tumors. A significant decrease in survival was detected for high versus low PGE, PGE + PGE deactivation products (PGEMs) and PGF in GBM patients. Our data show the potential importance of prostanoid metabolism in the progression towards GBM and provide evidence that higher PGE and PGF concentrations in the tumor are correlated with poorer patient survival. Our findings highlight the potential importance of the enzymes 15-HPGD and PTGR1 as prognostic biomarkers which could be used to predict survival outcome of patients with GBM.

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P424 Novel Biomarker for Hepatocellular Carcinoma: The Antioxidant Response in the Carcinogenesis

Cited by 2 publications

References 0 publications

RNAseq Analysis of Treatment-dependent Signaling Changes During Inflammation in a Mouse Cutaneous Wound Healing Model.

RNAseq Analysis of Treatment-dependent Signaling Changes During Inflammation in a Mouse Cutaneous Wound Healing Model.

The prostanoid pathway contains potential prognostic markers for glioblastoma

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