Poly (ADP-ribose) polymerase-1 inhibition decreases proliferation through G2/M arrest in esophageal squamous cell carcinoma

Yamamoto, Masaaki; Yamasaki, Makoto; Tsukao, Yukiko; Miyazaki, Yasuhiro; Makino, Tomoki; Takahashi, Tsuyoshi; Kurokawa, Yukinori; Nakajima, Kiyokazu; Takiguchi, Shuji; Mori, Masaki; Doki, Yuichiro

doi:10.3892/ol.2017.6334

Cited by 9 publications

(14 citation statements)

References 21 publications

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“…It is well known that the core of the cell cycle regulation mechanism is a group of cell cycle dependent protein kinase (CDKs), which is dependent on their regulatory subunit cyclins. Cyclin E and CDK2 are major regulators of cell cycle checkpoint and their interaction triggers the entry into the S phase, while cyclin B1‐CDK1 is potential to promote cell cycle progression from the S phase to G 2 /M phase . ADP has been reported to inhibit proliferation of the human lung adenocarcinoma cells via the induction of massive accumulation of cells in the S phase .…”

Section: Discussionmentioning

confidence: 99%

Adenosine diphosphate–sensitive P2Y11 receptor inhibits endothelial cell proliferation by induction of cell cycle arrest in the S phase and induces the expression of inflammatory mediators

Chen

Xiao

Yang

et al. 2018

J of Cellular Biochemistry

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Extracellular adenosine diphosphate (ADP) mediates a wide range of physiological effects as an extracellular signaling molecule, including platelet aggregation, vascular tone, cell proliferation, and apoptosis by interacting with plasma membrane P2 receptors. However, the effect of ADP on cell proliferation was contradictory. In this study, we found that ADP significantly inhibited cell proliferation of human umbilical vein endothelial cells at high concentrations (50 to 100 µM). Treatment with ADP did not induce cell apoptosis but instead induced cell cycle arrest in the S phase, which may be partly due to the downregulation of cyclin B1. The inhibition of cell proliferation was blocked by suramin, a nonspecific antagonist of the P2 receptors, and high concentrations of ADP significantly upregulated the messenger RNA (mRNA) and protein expression of P2Y11 in endothelial cells. Moreover, the downregulation of P2Y11 by RNA interference reversed the inhibition of cell proliferation. In addition, ADP (100 µM) can induce the formation of cytosolic autophagy in endothelial cells and a rapid phosphorylation of extracellular signal regulated kinase (ERK) 1/2, which is a canonical signal molecule downstream of P2Y receptors, accompanied by a mRNA expression of proinflammatory cytokines such as intercellular adhesion molecule 1 and vascular cell adhesion molecule 1. Taken together, our study excludes a mechanism for extracellular ADP impairing endothelial cells proliferation via P2Y11 receptor by downregulating cyclin B1 and arresting cell cycle at the S phase, besides, ADP induces cell autophagy and mRNA expression of inflammatory cytokines, whether it is mediated by Erk signaling pathways needs further studies to confirm.

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Section: Discussionmentioning

confidence: 99%

Adenosine diphosphate–sensitive P2Y11 receptor inhibits endothelial cell proliferation by induction of cell cycle arrest in the S phase and induces the expression of inflammatory mediators

Chen

Xiao

Yang

et al. 2018

J of Cellular Biochemistry

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“…25 In addition, a Phase II study of the EGFR tyrosine kinase inhibitor icotinib reported a 16.6% overall response rate (ORR) and a 46.3% disease control rate in oesophageal squamous cell carcinomas with either high EGFR expression on IHC or amplification on FISH. 26 Based on laboratory studies of oesophageal squamous cell carcinoma, several other potential novel therapeutic targets exist, 20 including CDK4/6, 27 poly (ADP-ribose) polymerase-1 (PARP), 28,29 the NRF2 signalling pathway 30 and the Wnt signalling pathway. 31 However, given current treatment guidelines, pathologists have little role to play regarding targeted therapy for oesophageal squamous cell carcinoma other than outside PD-L1 immunohistochemical staining, if requested.…”

Section: Oesophageal Squamous Cell Carcinomamentioning

confidence: 99%

“…Based on laboratory studies of oesophageal squamous cell carcinoma, several other potential novel therapeutic targets exist, 20 including CDK4/6, 27 poly(ADP‐ribose) polymerase‐1 (PARP), 28,29 the NRF2 signalling pathway 30 and the Wnt signalling pathway 31 . However, given current treatment guidelines, pathologists have little role to play regarding targeted therapy for oesophageal squamous cell carcinoma other than outside PD‐L1 immunohistochemical staining, if requested.…”

Section: Oesophageal Squamous Cell Carcinomamentioning

confidence: 99%

Targeted therapy for upper gastrointestinal tract cancer: current and future prospects

Rosenbaum

González

2020

Histopathology

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Gastric and oesophageal carcinoma remain major causes of worldwide mortality and morbidity. Despite incredible progress in understanding tumour biology, few targeted treatment options have proved effective in prolonging survival, and adjuvant therapy is largely interchangeable in these carcinomas. Through large‐scale sequencing by the Cancer Genome Atlas and the Asian Cancer Research Group, numerous potential molecular targets have been discovered. Of the approved targeted therapies for gastric and oesophageal cancer, pathologists play a role in patient selection for the majority of them. Trastuzumab has been approved as a first‐line therapy in conjunction with standard treatment in adenocarcinomas with either 3+ HER2/neu expression by immunohistochemistry or ERBB2 amplification by FISH. PD‐L1 immunohistochemistry showing a combined positive score of 1 or greater qualifies patients for third‐line pembrolizumab therapy, and identification of microsatellite instability‐high carcinomas may qualify patients for second‐line pembrolizumab. Ramucirumab, targeting VEGFR2, has also been approved for second‐line therapy in gastric carcinoma. Non‐surgical therapy for gastrointestinal stromal tumours relies mainly upon tyrosine kinase inhibitors, while new targeted therapy options for neuroendocrine neoplasms have recently emerged. Potential future options for targeted therapy in all these malignancies are being investigated in clinical trials, as this review will discuss.

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“…In general, ADP-ribosyltransferases are responsible for regulation of intracellular and extracellular signal transduction. Therefore, their activity determines viability and proliferation potential of cells, DNA stability, immune system reactivity and thus the proper functioning of eukaryotic organisms ( Bai, 2015 ; Corda & Di Girolamo, 2002 ; De Vos, Schreiber & Dantzer, 2012 ; Yamamoto et al, 2017 ). On the other hand, ADP-ribosyltransferases may also be involved in development of pathological states such as neurodegenerative disorders, diabetes, atherosclerosis, cataract and cancer ( Barreiro & Gea, 2018 ; Gunderson & Moore, 2015 ; Kamboj et al, 2013 ; Malyuchenko et al, 2015 ; Mangerich & Bürkle, 2012 ; Rossi, Ghosh & Bohr, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

A novel predicted ADP-ribosyltransferase-like family conserved in eukaryotic evolution

Wyżewski

Gradowski

Krysińska

et al. 2021

PeerJ

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The presence of many completely uncharacterized proteins, even in well-studied organisms such as humans, seriously hampers full understanding of the functioning of the living cells. ADP-ribosylation is a common post-translational modification of proteins; also nucleic acids and small molecules can be modified by the covalent attachment of ADP-ribose. This modification, important in cellular signalling and infection processes, is usually executed by enzymes from the large superfamily of ADP-ribosyltransferases (ARTs). Here, using bioinformatics approaches, we identify a novel putative ADP-ribosyltransferase family, conserved in eukaryotic evolution, with a divergent active site. The hallmark of these proteins is the ART domain nestled between flanking leucine-rich repeat (LRR) domains. LRRs are typically involved in innate immune surveillance. The novel family appears as putative novel ADP-ribosylation-related actors, most likely pseudoenzymes. Sequence divergence and lack of clearly detectable “classical” ART active site suggests the novel domains are pseudoARTs, yet atypical ART activity, or alternative enzymatic activity cannot be excluded. We propose that this family, including its human member LRRC9, may be involved in an ancient defense mechanism, with analogies to the innate immune system, and coupling pathogen detection to ADP-ribosyltransfer or other signalling mechanisms.

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Poly (ADP-ribose) polymerase-1 inhibition decreases proliferation through G2/M arrest in esophageal squamous cell carcinoma

Cited by 9 publications

References 21 publications

Adenosine diphosphate–sensitive P2Y11 receptor inhibits endothelial cell proliferation by induction of cell cycle arrest in the S phase and induces the expression of inflammatory mediators

Adenosine diphosphate–sensitive P2Y11 receptor inhibits endothelial cell proliferation by induction of cell cycle arrest in the S phase and induces the expression of inflammatory mediators

Targeted therapy for upper gastrointestinal tract cancer: current and future prospects

A novel predicted ADP-ribosyltransferase-like family conserved in eukaryotic evolution

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