scholarly journals A Review of Auraptene as an Anticancer Agent

2021 ◽  
Vol 12 ◽  
Author(s):  
Zahra Tayarani-Najaran ◽  
Nilufar Tayarani-Najaran ◽  
Samira Eghbali
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Cellular Proliferation ◽  
Control Cell ◽  
Aberrant Crypt Foci ◽  
Glutathione S Transferase ◽  
Anticancer Effects ◽  
Anti Oxidant ◽  
Anti Fungal ◽  
Cell Signaling Pathways

Auraptene is a bioactive monoterpene coumarin isolated from Citrus aurantium and Aegle marmelos that belong to the Rutaceae family. Auraptene can modulate intracellular signaling pathways that control cell growth, inflammation and apoptosis and can exert pharmacological properties such as anti-bacterial, anti-fungal, antileishmania and anti-oxidant activity. Auraptene had inhibitory and chemo-preventive effects on the proliferation, tumorigenesis and growth of several cancer cell lines through increase in the activity of glutathione S-transferase, formation of DNA adducts and reduction of the number of aberrant crypt foci. Auraptene exhibits anticancer effects via targeting different cell signaling pathways such as cytokines, genes modulating cellular proliferation, growth factors, transcription factors and apoptosis. The present review is a detailed survey of scientific researches on the cytotoxicity and anticancer activity of Auraptene on cancer cells and tumor bearing animals.

scholarly journals Interplay between ADP-ribosyltransferases and essential cell signaling pathways controls cellular responses

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Flurina Boehi ◽  
Patrick Manetsch ◽  
Michael O. Hottiger
Keyword(s):  
Cell Signaling ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Cellular Responses ◽  
Dynamic Regulation ◽  
Post Translational Modifications ◽  
Adp Ribosylation ◽  
Cellular Processes ◽  
Adp Ribosyltransferase ◽  
Cell Signaling Pathways

AbstractSignaling cascades provide integrative and interactive frameworks that allow the cell to respond to signals from its environment and/or from within the cell itself. The dynamic regulation of mammalian cell signaling pathways is often modulated by cascades of protein post-translational modifications (PTMs). ADP-ribosylation is a PTM that is catalyzed by ADP-ribosyltransferases and manifests as mono- (MARylation) or poly- (PARylation) ADP-ribosylation depending on the addition of one or multiple ADP-ribose units to protein substrates. ADP-ribosylation has recently emerged as an important cell regulator that impacts a plethora of cellular processes, including many intracellular signaling events. Here, we provide an overview of the interplay between the intracellular diphtheria toxin-like ADP-ribosyltransferase (ARTD) family members and five selected signaling pathways (including NF-κB, JAK/STAT, Wnt-β-catenin, MAPK, PI3K/AKT), which are frequently described to control or to be controlled by ADP-ribosyltransferases and how these interactions impact the cellular responses.

scholarly journals Extracellular matrix in cardiovascular pathophysiology

2018 ◽  
Vol 315 (6) ◽  
pp. H1687-H1690 ◽  
Author(s):  
Maria Bloksgaard ◽  
Merry Lindsey ◽  
Luis A. Martinez-Lemus
Keyword(s):  
Extracellular Matrix ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Physical And Mechanical Properties ◽  
Disease Development ◽  
Cardiovascular Development ◽  
Intracellular Signaling Pathways ◽  
Circulatory Physiology ◽  
Activate Cell ◽  
Cell Signaling Pathways

The extracellular matrix (ECM) actively participates in diverse aspects of cardiovascular development and physiology as well as during disease development and progression. ECM roles are determined by its physical and mechanical properties and by its capacity to both release bioactive signals and activate cell signaling pathways. The ECM serves as a storage depot for a wide variety of molecules released in response to injury or with aging. Indeed, there is a plethora of examples describing how cells react to or modify ECM stiffness, how cells initiate intracellular signaling pathways, and how cells respond to the ECM. This Perspectives article reviews the contributions of 21 articles published in the American Journal of Physiology-Heart and Circulatory Physiology in response to a Call for Papers on this topic. Here, we summarize the contributions of these studies focused on the cardiac and vascular ECM. We highlight the translational importance of these studies and conclude that the ECM is a critical component of both the heart and vasculature. Readers are urged to examine and learn from this special Call for Papers.

Cerium oxide nanoparticles and their importance in cell signaling pathways for predicting cellular behavior

Nanomedicine ◽  
2020 ◽  
Vol 15 (17) ◽  
pp. 1709-1718
Author(s):  
Atefeh Pesaraklou ◽  
Maryam M Matin
Keyword(s):  
Signaling Pathways ◽  
Cerium Oxide ◽  
Cellular Responses ◽  
Cerium Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Signaling Proteins ◽  
Cellular Behavior ◽  
Anti Oxidant ◽  
Different Response ◽  
Cell Signaling Pathways

Cerium oxide nanoparticles (CeO2-NPs) have prolifically attracted immense interest of researchers due to their prominent anti-oxidant nature. However, these characteristics are accompanied by some ambiguities in other studies reporting their oxidant and toxic properties. In this regard previous literature has pointed to the importance of the NPs morphology and environmental conditions as well as biomolecules that induce a different response by initiating a cascade of activities. Therefore, due to the fact that signaling proteins are key mediators in cellular responses, the cognizance of the CeO2-NP-targeted signaling pathways could facilitate predicting the cellular behavior and thus more efficient applications of these NPs for clinical purposes. Consequently, a comprehensive review is necessary in this field, to clarify the impacts of CeO2-NPs on various signaling pathways.

Cucurbitacins: A Systematic Review of the Phytochemistry and Anticancer Activity

2015 ◽  
Vol 43 (07) ◽  
pp. 1331-1350 ◽  
Author(s):  
Yuee Cai ◽  
Xiefan Fang ◽  
Chengwei He ◽  
Peng Li ◽  
Fei Xiao ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Mapk Signaling ◽  
Research Progress ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
And Migration

Cucurbitacins are highly oxidized tetracyclic triterpenoids that are widely present in traditional Chinese medicines (Cucurbitaceae family), possess strong anticancer activity, and are divided into 12 classes from A to T with over 200 derivatives. The eight most active cucurbitacin components against cancer are cucurbitacin B, D, E, I, IIa, L glucoside, Q, and R. Their mechanisms of action include antiproliferation, inhibition of migration and invasion, proapoptosis, and cell cycle arrest promotion. Cucurbitacins are also found to be the inhibitors of JAK-STAT3, Wnt, PI3K/Akt, and MAPK signaling pathways, which play important roles in the apoptosis and survival of cancer cells. Recently, new studies have discovered synergistic anticancer effects by using cucurbitacins together with clinically approved chemotherapeutic drugs, such as docetaxel and methotrexate. This paper provides a summary of recent research progress on the anticancer property of cucurbitacins and the various intracellular signaling pathways involved in the regulation of cancer cell proliferation, death, invasion, and migration. Therefore, cucurbitacins are a class of promising anticancer drugs to be used alone or be intergraded in current chemotherapies and radiotherapies to treat many types of cancers.

Sprouty: a common antagonist of FGF and EGF signaling pathways in Drosophila

Development ◽  
1999 ◽  
Vol 126 (11) ◽  
pp. 2515-2525 ◽  
Author(s):  
S. Kramer ◽  
M. Okabe ◽  
N. Hacohen ◽  
M.A. Krasnow ◽  
Y. Hiromi
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Cellular Proliferation ◽  
Egf Receptor ◽  
Ovarian Follicle ◽  
Follicle Cells ◽  
Chordotonal Organ ◽  
Fgf Signaling ◽  
Tracheal System ◽  
Egf Signaling

Extracellular factors such as FGF and EGF control various aspects of morphogenesis, patterning and cellular proliferation in both invertebrates and vertebrates. In most systems, it is primarily the distribution of these factors that controls the differential behavior of the responding cells. Here we describe the role of Sprouty in eye development. Sprouty is an extracellular protein that has been shown to antagonize FGF signaling during tracheal branching in Drosophila. It is a novel type of protein with a highly conserved cysteine-rich region. In addition to the embryonic tracheal system, sprouty is also expressed in other tissues including the developing eye imaginal disc, embryonic chordotonal organ precursors and the midline glia. In each of these tissues, EGF receptor signaling is known to participate in the control of the correct number of neurons or glia. We show that, in all three tissues, the loss of sprouty results in supernumerary neurons or glia, respectively. Furthermore, overexpression of sprouty in wing veins and ovarian follicle cells, two other tissues where EGF signaling is required for patterning, results in phenotypes that resemble the loss-of-function phenotypes of Egf receptor. These results suggest that Sprouty acts as an antagonist of EGF as well as FGF signaling pathways. These receptor tyrosine kinase-mediated pathways may share not only intracellular signaling components but also extracellular factors that modulate the strength of the signal.

Transcriptional Regulation of Thrombopoiesis.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. sci-38-sci-38
Author(s):  
Alan B. Cantor ◽  
Hui Huang ◽  
Andrew Woo ◽  
James Mann ◽  
Ming Yu ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Transcriptional Activation ◽  
Protein Complex ◽  
Molecular Mechanisms ◽  
Control Cell ◽  
Cell Fate Decisions ◽  
Platelet Disorder ◽  
Cell Signaling Pathways

Abstract Over the past two decades, a number of key transcription factors have been identified that play essential roles in megakaryocyte development. These include GATA-1, GATA-2, Friend of GATA-1 (FOG-1), Runx-1, Cbf-β, Fli-1, GABPα, TEL, NF-E2 p45, Gfi-1b, and SCL/TAL. Importantly, mutations in genes encoding several of these have been linked to human disorders of thrombopoieisis. Germline GATA-1 mutations that disrupt binding to FOG-1 cause X-linked macrothrombocytopenia and dyserythropoietic anemia. Acquired GATA-1 mutations that lead to exclusive production of a short isoform (GATA-1s) play initiating roles in Down Syndrome Transient Myeloproliferative Disorder (DS-TMD) and subsequent Acute Megakaryoblastic Leukemia (DS-AMKL). Haploinsufficiency of Runx-1 causes Familial Platelet Disorder with Propensity to Develop AML (FPD/ AML). Heterozygous loss of the Fli-1 gene leads to the macrothrombocytopenia seen in Jacobsen’s (Paris-Trousseau) syndrome. Important outstanding questions include: how these transcription factors act together to control megakaryocyte terminal maturation; how they differentially act as activators or repressors depending on gene context; how they intersect with cell signaling pathways; how they may coordinate terminal megakaryocyte maturation with spatial location within the bone marrow; how they may control cell fate decisions of bipotential erythroid/megakaryocytic progenitor cells; and whether additional key transcription factors exist. Application of proteomic approaches involving multi-protein complex purification has provided novel insights into some of these questions. We have isolated GATA-1 containing complexes from megakaryocytic cells and identified the Krüppel-type zinc finger transcription factor ZBP-89 as a novel regulator of megakaryocyte and erythroid development. Knockdown of ZBP-89 expression in zebrafish embryos and mice results in blocked early megakaryopoiesis and definitive erythropoiesis, phenocopying aspects of GATA-1- and FOG-1-deficient animals. We have also found that the focal adhesion component Kindlin-3 co-localizes to the nucleus and interacts with FOG-1, suggesting a possible link between integrin signaling and megakaryocyte transcriptional control. Runx-1 multi-protein complex purifications have led to the identification of Fli-1 as a direct binding partner. This interaction results in synergistic transcriptional activation of megakaryocyte-specific genes. Interestingly, the interaction between Runx-1 and Fli-1 occurs preferentially in cells that are differentiating, even though both proteins are expressed abundantly in undifferentiated megakaryoblastic cells. This binding event correlates with assembly of a large complex containing Runx-1/ Fli-1/GATA-1/FOG-1 based on gel filtration chromatography experiments. These factors may, therefore, act as a megakaryocyte-specific enhancesome. Key future directions are aimed at elucidating the molecular mechanisms that regulate these protein-protein interactions and how cell signaling pathways may modulate them.

scholarly journals Helicobacter pylori-Mediated Immunity and Signaling Transduction in Gastric Cancer

2020 ◽  
Vol 9 (11) ◽  
pp. 3699
Author(s):  
Nozomi Ito ◽  
Hironori Tsujimoto ◽  
Hideki Ueno ◽  
Qian Xie ◽  
Nariyoshi Shinomiya
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Intracellular Signaling ◽  
Cellular Proliferation ◽  
Gastric Cancer Cells ◽  
Downstream Signaling ◽  
H Pylori

Helicobacter pylori infection is a leading cause of gastric cancer, which is the second-most common cancer-related death in the world. The chronic inflammatory environment in the gastric mucosal epithelia during H. pylori infection stimulates intracellular signaling pathways, namely inflammatory signals, which may lead to the promotion and progression of cancer cells. We herein report two important signal transduction pathways, the LPS-TLR4 and CagA-MET pathways. Upon H. pylori stimulation, lipopolysaccharide (LPS) binds to toll-like receptor 4 (TLR4) mainly on macrophages and gastric epithelial cells. This induces an inflammatory response in the gastric epithelia to upregulate transcription factors, such as NF-κB, AP-1, and IRFs, all of which contribute to the initiation and progression of gastric cancer cells. Compared with other bacterial LPSs, H. pylori LPS has a unique function of inhibiting the mononuclear cell (MNC)-based production of IL-12 and IFN-γ. While this mechanism reduces the degree of inflammatory reaction of immune cells, it also promotes the survival of gastric cancer cells. The HGF/SF-MET signaling plays a major role in promoting cellular proliferation, motility, migration, survival, and angiogenesis, all of which are essential factors for cancer progression. H. pylori infection may facilitate MET downstream signaling in gastric cancer cells through its CagA protein via phosphorylation-dependent and/or phosphorylation-independent pathways. Other signaling pathways involved in H. pylori infection include EGFR, FAK, and Wnt/β-Catenin. These pathways function in the inflammatory process of gastric epithelial mucosa, as well as the progression of gastric cancer cells. Thus, H. pylori infection-mediated chronic inflammation plays an important role in the development and progression of gastric cancer.

scholarly journals Optogenetic control of cell morphogenesis on protein micropatterns

2019 ◽  
Author(s):  
Katja Zieske ◽  
R Dyche Mullins
Keyword(s):  
Signaling Pathways ◽  
Adhesion Molecules ◽  
Intracellular Signaling ◽  
Control Cell ◽  
Tissue Formation ◽  
Actin Assembly ◽  
Cell Morphogenesis ◽  
Cell Protrusion ◽  
Cytoskeletal Dynamics ◽  
Membrane Protrusions

AbstractCell morphogenesis is critical for embryonic development, tissue formation, and wound healing. Our ability to manipulate endogenous mechanisms to control cell shape, however, remains limited. Here we combined surface micropatterning of adhesion molecules with optogenetic activation of intracellular signaling pathways to control the nature and morphology of cellular protrusions. We employed geometry-dependent pre-organization of cytoskeletal structures together with acute activation of signaling pathways that control actin assembly to create a tool capable of generating membrane protrusions at defined cellular locations. Further, we find that the size of microfabricated patterns of adhesion molecules influences the molecular mechanism of cell protrusion: larger patterns enable cells to create actin-filled lamellipodia while smaller patterns promote formation of spherical blebs. Optogenetic perturbation of signaling pathways in these cells changes the size of blebs and convert them into lamellipodia. Our results demonstrate how the coordinated manipulation of adhesion geometry and cytoskeletal dynamics can be used to control membrane protrusion and cell morphogenesis.

scholarly journals Roles of mTOR in thoracic aortopathy understood by complex intracellular signaling interactions

2021 ◽  
Vol 17 (12) ◽  
pp. e1009683
Author(s):  
Ana C. Estrada ◽  
Linda Irons ◽  
Bruno V. Rego ◽  
Guangxin Li ◽  
George Tellides ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Signaling ◽  
Smooth Muscle Cell ◽  
Signaling Pathways ◽  
Muscle Cell ◽  
Intracellular Signaling ◽  
Cellular Mechanisms ◽  
Data Set ◽  
Bistable Switch ◽  
Cell Signaling Pathways

Thoracic aortopathy–aneurysm, dissection, and rupture–is increasingly responsible for significant morbidity and mortality. Advances in medical genetics and imaging have improved diagnosis and thus enabled earlier prophylactic surgical intervention in many cases. There remains a pressing need, however, to understand better the underlying molecular and cellular mechanisms with the hope of finding robust pharmacotherapies. Diverse studies in patients and mouse models of aortopathy have revealed critical changes in multiple smooth muscle cell signaling pathways that associate with disease, yet integrating information across studies and models has remained challenging. We present a new quantitative network model that includes many of the key smooth muscle cell signaling pathways and validate the model using a detailed data set that focuses on hyperactivation of the mechanistic target of rapamycin (mTOR) pathway and its inhibition using rapamycin. We show that the model can be parameterized to capture the primary experimental findings both qualitatively and quantitatively. We further show that simulating a population of cells by varying receptor reaction weights leads to distinct proteomic clusters within the population, and that these clusters emerge due to a bistable switch driven by positive feedback in the PI3K/AKT/mTOR signaling pathway.

scholarly journals The Multifaceted Therapeutic Mechanisms of Curcumin in Osteosarcoma: State-of-the-Art

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Fatemeh Zahedipour ◽  
Monireh Bolourinezhad ◽  
Yong Teng ◽  
Amirhossein Sahebkar
Keyword(s):  
Survival Time ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Curcuma Longa ◽  
Potential Candidate ◽  
Anti Cancer ◽  
Adults And Children ◽  
Anti Oxidant ◽  
Therapeutic Mechanisms

Osteosarcoma is a major form of malignant bone tumor that typically occurs in young adults and children. The combination of aggressive surgical strategies and chemotherapy has led to improvements in survival time, although individuals with recurrent or metastatic conditions still have an extremely poor prognosis. This disappointing situation strongly indicates that testing novel, targeted therapeutic agents is imperative to prevent the progression of osteosarcoma and enhance patient survival time. Curcumin, a naturally occurring phenolic compound found in Curcuma longa, has been shown to have a wide variety of anti-tumor, anti-oxidant, and anti-inflammatory activities in many types of cancers including osteosarcoma. Curcumin is a highly pleiotropic molecule that can modulate intracellular signaling pathways to regulate cell proliferation, inflammation, and apoptosis. These signaling pathways include RANK/RANKL, Notch, Wnt/β-catenin, apoptosis, autophagy, JAK/STAT, and HIF-1 pathways. Additionally, curcumin can regulate the expression of various types of microRNAs that are involved in osteosarcoma. Therefore, curcumin may be a potential candidate for the prevention and treatment of osteosarcoma. This comprehensive review not only covers the use of curcumin in the treatment of osteosarcoma and its anti-cancer molecular mechanisms but also reveals the novel delivery strategies and combination therapies with the aim to improve the therapeutic effect of curcumin.

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