Inhibitory role of oleanolic acid and esculetin in HeLa cells involve multiple signaling pathways

Gene ◽  
2021 ◽  
Vol 771 ◽  
pp. 145370
Author(s):  
Prajitha Mohandas Edathara ◽  
Shivakanth Chintalapally ◽  
Venkata Krishna Kanth Makani ◽  
Chitrakshi Pant ◽  
Suresh Yerramsetty ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Oleanolic Acid ◽  
Hela Cells ◽  
Inhibitory Role ◽  
Multiple Signaling

scholarly journals Extracellular ATP plays an important role in systemic wound response activation

2022 ◽  
Author(s):  
Ronald Myers ◽  
Yosef Fichman ◽  
Gary Stacey ◽  
Ron Mittler
Keyword(s):  
Signaling Pathways ◽  
Extracellular Atp ◽  
Wound Response ◽  
Mechanical Wounding ◽  
Long Distance ◽  
Wound Responses ◽  
Systemic Signal ◽  
Electric Signals ◽  
Multiple Signaling

Mechanical wounding occurs in plants during biotic (e.g., herbivore or pathogen attack) or abiotic (e.g., wind damage or freezing) stresses and is associated with the activation of multiple signaling pathways. These initiate many wound responses at the wounded tissues, as well as trigger long-distance signaling pathways that activate wound responses in tissues that were not affected by the initial wounding event (termed systemic wound response). Among the different systemic signals activated by wounding are electric signals, calcium and reactive oxygen species (ROS) waves, and different plant hormones such as jasmonic acid. The release of glutamate from cells at the wounded tissues was recently proposed to trigger several different systemic signal transduction pathways via glutamate-like receptors (GLRs). However, the role of another important compound released from cells during wounding (i.e., extracellular ATP; eATP) in triggering systemic responses is not clear. Here we show that eATP that accumulates in wounded leaves and is sensed by the purinoreceptor kinase P2K is required for the activation of the ROS wave during wounding. Application of eATP to unwounded leaves triggered the ROS wave, and the activation of the ROS wave by wounding or eATP application was suppressed in mutants deficient in P2K (i.e., p2k1-3, p2k2, and p2k1-3p2k2). In addition, the expression of several systemic wound response transcripts was suppressed in mutants deficient in P2K during wounding. Our findings reveal that in addition to sensing glutamate via GLRs, eATP sensed by P2Ks is playing a key role in the triggering of systemic wound responses in plants.

scholarly journals Oxidative Stress and Cancer: Chemopreventive and Therapeutic Role of Triphala

Antioxidants ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 72 ◽  
Author(s):  
Sahdeo Prasad ◽  
Sanjay K. Srivastava
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Signaling Pathways ◽  
Multiple Cell ◽  
Multiple Signaling ◽  
Immense Potential ◽  
Cell Signaling Pathways ◽  
Radioprotective Agent

Oxidative stress, caused by the overproduction of free radicals, leads to the development of many chronic diseases including cancer. Free radicals are known to damage cellular biomolecules like lipids, proteins, and DNA that results in activation of multiple signaling pathways, growth factors, transcription factors, kinases, inflammatory and cell cycle regulatory molecules. Antioxidants, which are classified as exogenous and endogenous, are responsible for the removal of free radicals and consequently the reduction in oxidative stress-mediated diseases. Diet and medicinal herbs are the major source of antioxidants. Triphala, which is a traditional Ayurvedic formulation that has been used for centuries, has been shown to have immense potential to boost antioxidant activity. It scavenges free radicals, restores antioxidant enzymes and non-enzyme levels, and decreases lipid peroxidation. In addition, Triphala is revered as a chemopreventive, chemotherapeutic, immunomodulatory, and radioprotective agent. Accumulated evidence has revealed that Triphala modulates multiple cell signaling pathways including, ERK, MAPK, NF-κB, Akt, c-Myc, VEGFR, mTOR, tubulin, p53, cyclin D1, anti-apoptotic and pro-apoptotic proteins. The present review focuses on the comprehensive appraisal of Triphala in oxidative stress and cancer.

scholarly journals p-21-Activated kinase 1 mediates gastrin-stimulated proliferation in the colorectal mucosa via multiple signaling pathways

2013 ◽  
Vol 304 (6) ◽  
pp. G561-G567 ◽  
Author(s):  
Nhi Huynh ◽  
Mildred Yim ◽  
Jonathan Chernoff ◽  
Arthur Shulkes ◽  
Graham S. Baldwin ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Control Cell ◽  
Growth Factor Signaling ◽  
Extracellular Signal Regulated Kinase ◽  
Colorectal Mucosa ◽  
Extracellular Signal ◽  
And Migration ◽  
Multiple Signaling

Gastrins, including amidated (Gamide) and glycine-extended (Ggly) forms, function as growth factors for the gastrointestinal mucosa. The p-21-activated kinase 1 (PAK1) plays important roles in growth factor signaling networks that control cell motility, proliferation, differentiation, and transformation. PAK1, activated by both Gamide and Ggly, mediates gastrin-stimulated proliferation and migration, and activation of β-catenin, in gastric epithelial cells. The aim of this study was to investigate the role of PAK1 in the regulation by gastrin of proliferation in the normal colorectal mucosa in vivo. Mucosal proliferation was measured in PAK1 knockout (PAK1 KO) mice by immunohistochemistry. The expression of phosphorylated and unphosphorylated forms of the signaling molecules PAK1, extracellular signal-regulated kinase (ERK), and protein kinase B (AKT), and the expression of β-catenin and its downstream targets c-Myc and cyclin D1, were measured in gastrin knockout (Gas KO) and PAK1 KO mice by Western blotting. The expression and activation of PAK1 are decreased in Gas KO mice, and these decreases are associated with reduced activation of ERK, AKT, and β-catenin. Proliferation in the colorectal mucosa of PAK1 KO mice is reduced, and the reduction is associated with reduced activation of ERK, AKT, and β-catenin. In compensation, antral gastrin mRNA and serum gastrin concentrations are increased in PAK1 KO mice. These results indicate that PAK1 mediates the stimulation of colorectal proliferation by gastrins via multiple signaling pathways involving activation of ERK, AKT, and β-catenin.

scholarly journals The Role of Glypican-1 in Regulating Multiple Cellular Signaling Pathways

2021 ◽  
Author(s):  
Jiajia Pan ◽  
Mitchell Ho
Keyword(s):  
Cell Membrane ◽  
Cell Surface ◽  
Signaling Pathways ◽  
Core Protein ◽  
Specific Interactions ◽  
Domain Interaction ◽  
Glycosyl Phosphatidylinositol ◽  
The Impact ◽  
Multiple Signaling

Glypican-1 (GPC1) is one of the six glypican family members in humans. It is composed of a core protein with three heparan sulfate chains, and attached to the cell membrane by a glycosyl-phosphatidylinositol anchor. GPC1 modulates various signaling pathways including FGF, VEGF-A, TGF-β, Wnt, Hh, and BMP through specific interactions with pathway ligands and receptors. The impact of these interactions on signaling pathways, activating or inhibitory, is dependent upon specific GPC1 domain interaction with pathway components as well as cell surface context. In this review, we summarize the current understanding of the structure of GPC1, as well as its role in regulating multiple signaling pathways. We focus on the functions of GPC1 in cancer cells and how new insights into these signaling processes can inform its translational potential as a therapeutic target in cancer.

scholarly journals Initial effects of inflammation-related cytokines and signaling pathways on the pathogenesis of post-traumatic osteoarthritis

2018 ◽  
Vol 5 (2) ◽  
pp. 91-96
Author(s):  
Peng-Fei Han ◽  
Zhi-Liang Zhang ◽  
Tao-Yu Chen ◽  
Rui-Peng Zhao ◽  
Rong Zhang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cartilage Degeneration ◽  
Pathological Process ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Post Traumatic ◽  
Multiple Signaling ◽  
The Relationship ◽  
And Oxidative Stress

Abstract The main pathological change in post-traumatic osteoarthritis (PTOA) is cartilage degeneration, which is closely related to inflammation and oxidative stress. Inflammation can cause degeneration of articular cartilage. Cartilage degeneration can also stimulate the progression of inflammation. It has been found that inflammatory cytokines can participate in the pathological process of cartilage degeneration through multiple signaling pathways, mainly mitogen-activated protein kinase, nuclear transcription factor kappa B, and Wnt–β-catenin signal transduction pathways. This review aimed at exploring the relationship between PTOA and inflammation-related cytokines by introducing the role of proinflammatory cytokines in chondrocyte destruction and extracellular matrix degradation.

scholarly journals The Role of CTHRC1 in Regulation of Multiple Signaling and Tumor Progression and Metastasis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Dan Mei ◽  
Yue Zhu ◽  
Lingling Zhang ◽  
Wei Wei
Keyword(s):  
Signaling Pathways ◽  
Cellular Localization ◽  
Cancer Colorectal ◽  
Early Stage ◽  
Small Cell Lung Carcinoma ◽  
Cell Lung Carcinoma ◽  
Collagen Triple Helix ◽  
Adventitial Fibroblasts ◽  
Multiple Signaling

Collagen triple helix repeat containing-1 (CTHRC1) has been identified as cancer-related protein. CTHRC1 expresses mainly in adventitial fibroblasts and neointimal smooth muscle cells of balloon-injured vessels and promotes cell migration and tissue repair in response to injury. CTHRC1 plays a pivotal role in some pathophysiological processes, including increasing bone mass, preventing myelination, and reversing collagen synthesis in many tumor cells. The ascended expression of CTHRC1 is related to tumorigenesis, proliferation, invasion, and metastasis in various human malignancies, including gastric cancer, pancreatic cancer, hepatocellular carcinoma, keloid, breast cancer, colorectal cancer, epithelial ovarian cancer, esophageal squamous cell carcinoma, cervical cancer, non-small-cell lung carcinoma, and melanoma. And molecules that regulate the expression of CTHRC1 include miRNAs, lncRNAs, WAIF1, and DPAGT1. Many reports have pointed that CTHRC1 could exert different effects through several signaling pathways such as TGF-β, Wnt, integrin β/FAK, Src/FAK, MEK/ERK, PI3K/AKT/ERK, HIF-1α, and PKC-δ/ERK signaling pathways. As a participant in tissue remodeling or immune response, CTHRC1 may promote early-stage cancer. Several recent studies have identified CTHRC1 as an effectual prognostic biomarker for predicting tumor recurrence or metastasis. It is worth noting that CTHRC1 has different cellular localization and mechanisms of action in different cells and different microenvironments. In this article, we focus on the advances in the signaling pathways mediated by CTHRC1 in tumors.

Sign in / Sign up

Export Citation Format

Share Document