Decreasing P-selectin and ICAM-1 via activating Akt: a possible mechanism by which PARG inhibits adhesion of mouse colorectal carcinoma CT26 cells to platelets

Yan, Jingye; Li, M; Threadgill, Michael D.; Wang, Y; Fu, Wen‐Mei

doi:10.1038/cgt.2013.44

Cited by 4 publications

(3 citation statements)

References 38 publications

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“…Anti-inflammatory effect of 4R may also be due to enhancement or maintenance of Akt phosphorylation in brain endothelial cells under ischemic condition (Fig. 5C, 5D), because phosphorylation of Akt could inhibit inflammation by suppression of ICAM-1 and other inflammatory factors (Song et al, 2013; Yan et al, 2013; Zhu et al, 2003). These data provide further evidence in the mechanism of 4R protection in ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in rodent models of brain ischemia

Martins

et al. 2015

Neuroscience

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(1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) is a precursor to key flavor ingredients in leaves of Nicotiana species. The present study shows 4R decreased brain damage in rodent ischemic stroke models. The 4R-pretreated mice had lower infarct volume (26.2±9.7 mm3) than those in control groups (untreated: 63.4±4.2 mm3, DMSO: 60.2±14.2 mm3). The 4R-posttreated rats also had less infarct volume (120±65 mm3) than those in the rats of DMSO group (291±95 mm3). The results from in vitro experiments indicate that 4R decreased neuro2a cells (neuroblastoma cells) apoptosis induced by oxygen glucose deprivation (OGD), and improved the population spikes (PSs) recovery in rat acute hippocampal slices under OGD; a phosphatidylinositol 3-kinase (PI3K) inhibitor, wortmannin, abolished the effect of 4R on PSs recovery. Furthermore, 4R also inhibited monocyte adhesion to bEND5 cells (murine brain-derived endothelial cells) and upregulation of intercellular adhesion molecule-1(ICAM-1) induced by OGD/reoxygenation (OGD/R), and restored the p-Akt level to pre-OGD/R values in bEND5 cells. In conclusion, the present study indicates that 4R has a protective effect in rodent ischemic stroke models. Inhibition of ICAM-1 expression and restoration of Akt phosphorylation are the possible mechanisms involved in cellular protection by 4R.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in rodent models of brain ischemia

Martins

et al. 2015

Neuroscience

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“…Многочисленные данные, полученные на хирургическом материале пациентов с раком толстого кишечника (РТК) и клеточных линиях РТК человека (HT29, KM12) и мыши (CT26), свидетельствуют об экспрессии SiaLe x на поверхности клеток опухоли [33][34][35]. Экспрессия E-и P-селектинов была обнаружена как непосредственно на раковых клетках, так и на сосудистом микроокружении [36][37][38]. Данные об экспрессии селектинов и их лиганда SiaLe x в тканях при РТК представлены в таблице 3.…”

Section: селектины и Siale X при раке толстого кишечникаunclassified

Selectins of Tumor Cells and Vascular Microenviroment as Targets for Anti-Cancer Drug Delivery

Aronov¹,

Shubernetskaya²,

Semushina³

et al. 2022

СПНО (MPSE)

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Targeted therapy is promising for the treatment of malignant neoplasms. To date, one of the most common approaches for targeted drug delivery is the targeting of a cytotoxic agent to tumor cell membrane antigens; however, intratumoral heterogeneity is a significant limitation for these drugs. The search for promising targets for the development of targeted delivery of cytotoxic drugs remains an urgent task for modern pharmacology. In this review, we consider selectins on the surface of tumor cells as potential targets for the targeted drugs development using a specific ligand, sialyl Lewis X tetrasaccharide (SiaLe x ). The expression of both selectins and their ligand SiaLe x is ubiquitous in normal tissues and in pathology. Here we review the expression of selectins in breast cancer, pancreatic cancer, and colon cancer tissues. In these types of cancer, a high expression of P-and E-selectins is observed not only on the membrane of tumor cells, but also on the surface of the de novo tumor vasculature cells, which suggests the therapeutic effect of targeted delivery drugs using the SiaLe x vector due to both direct and indirect mechanisms of tumor destruction. However, the high expression of selectins in tissues with chronic inflammation in cancer patients may be a limitation to apply this type of drugs to all patients.

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“…PARylation may be involved in the expression of cell adhesion molecules [ 78 ] that mediate interactions with platelets ( Figure 3 A). Silencing of PARG in CT26 colorectal carcinoma cells increases the phosphorylation of AKT and decreases the expression of NF-κB and the cell adhesion molecules, ICAM-1 and P-selectin [ 79 ]. The CTCs/DTCs educate neutrophils and monocytes in the vasculature with C–C motif chemokine 2 (CCL2) to enhance vascular permeability, facilitating transmigration after homing at a potential metastatic site.…”

Section: Role Of Parps In Hallmarks Related To the Interplay Between Cancer And Hostmentioning

confidence: 99%

The PARP Enzyme Family and the Hallmarks of Cancer Part 2: Hallmarks Related to Cancer Host Interactions

Demény

Virág

2021

Cancers

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Poly (ADP-ribose) polymerases (PARPs) modify target proteins with a single ADP-ribose unit or with a poly (ADP-ribose) (PAR) polymer. PARP inhibitors (PARPis) recently became clinically available for the treatment of BRCA1/2 deficient tumors via the synthetic lethality paradigm. This personalized treatment primarily targets DNA damage-responsive PARPs (PARP1–3). However, the biological roles of PARP family member enzymes are broad; therefore, the effects of PARPis should be viewed in a much wider context, which includes complex effects on all known hallmarks of cancer. In the companion paper (part 1) to this review, we presented the fundamental roles of PARPs in intrinsic cancer cell hallmarks, such as uncontrolled proliferation, evasion of growth suppressors, cell death resistance, genome instability, replicative immortality, and reprogrammed metabolism. In the second part of this review, we present evidence linking PARPs to cancer-associated inflammation, anti-cancer immune response, invasion, and metastasis. A comprehensive overview of the roles of PARPs can facilitate the identification of novel cancer treatment opportunities and barriers limiting the efficacy of PARPi compounds.

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Decreasing P-selectin and ICAM-1 via activating Akt: a possible mechanism by which PARG inhibits adhesion of mouse colorectal carcinoma CT26 cells to platelets

Cited by 4 publications

References 38 publications

Neuroprotective activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in rodent models of brain ischemia

Neuroprotective activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in rodent models of brain ischemia

Selectins of Tumor Cells and Vascular Microenviroment as Targets for Anti-Cancer Drug Delivery

The PARP Enzyme Family and the Hallmarks of Cancer Part 2: Hallmarks Related to Cancer Host Interactions

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