scholarly journals Protectin DX promotes epithelial injury repair and inhibits fibroproliferation partly via ALX/PI3K signalling pathway

2020 ◽  
Vol 24 (23) ◽  
pp. 14001-14012
Author(s):  
Jing‐Xiang Yang ◽  
Ming Li ◽  
Xin Hu ◽  
Jia‐Chao Lu ◽  
Qian Wang ◽  
...  
Keyword(s):  
Signalling Pathway ◽  
Epithelial Injury ◽  
Injury Repair ◽  
Pi3k Signalling ◽  
Protectin Dx

scholarly journals Fisetin ameliorates Ischemia re-oxygenation injury in H9c2 cardiomyocytes via targeting the PI3K signalling pathway

2021 ◽  
pp. 100094
Author(s):  
Bhavana Sivakumar ◽  
Sri Rahavi Boovarahan ◽  
Priyanka N Prem ◽  
Gino A Kurian
Keyword(s):  
Signalling Pathway ◽  
H9c2 Cardiomyocytes ◽  
Pi3k Signalling

Signalling through Class I PI3Ks in mammalian cells

2006 ◽  
Vol 34 (5) ◽  
pp. 647-662 ◽  
Author(s):  
P.T. Hawkins ◽  
K.E. Anderson ◽  
K. Davidson ◽  
L.R. Stephens
Keyword(s):  
Cell Growth ◽  
Cell Surface ◽  
Mammalian Cells ◽  
Small Gtpases ◽  
Signalling Pathway ◽  
Class I ◽  
Cell Surface Receptors ◽  
Activity Class ◽  
Surface Receptors ◽  
Pi3k Signalling

It is now accepted that activation of Class I PI3Ks (phosphoinositide 3-kinases) is one of the most important signal transduction pathways used by cell-surface receptors to control intracellular events. The receptors which access this pathway include those that recognize growth factors, hormones, antigens and inflammatory stimuli, and the cellular events known to be regulated include cell growth, survival, proliferation and movement. We have learnt a great deal about the family of Class I PI3K enzymes themselves and the structural adaptations which allow a variety of cell-surface receptors to regulate their activity. Class I PI3Ks synthesize the phospholipid PtdIns(3,4,5)P3 in the membranes in which they are activated, and it is now accepted that PtdIns(3,4,5)P3 and its dephosphorylation product PtdIns(3,4)P2 are messenger molecules which regulate the localization and function of multiple effectors by binding to their specific PH (pleckstrin homology) domains. The number of direct PtdIns(3,4,5)P3/PtdIns(3,4)P2 effectors which exist, even within a single cell, creates an extremely complex signalling web downstream of PI3K activation. Some key players are beginning to emerge, however, linking PI3K activity to specific cellular responses. These include small GTPases for the Rho and Arf families which regulate the cytoskeletal and membrane rearrangements required for cell movement, and PKB (protein kinase B), which has important regulatory inputs into the regulation of cell-cycle progression and survival. The importance of the PI3K signalling pathway in regulating the balance of decisions in cell growth, proliferation and survival is clear from the prevalence of oncogenes (e.g. PI3Kα) and tumour suppressors [e.g. the PtdIns(3,4,5)P3 3-phosphatase, PTEN (phosphatase and tensin homologue deleted on chromosome 10)] found in this pathway. The recent availability of transgenic mouse models with engineered defects in Class I PI3K signalling pathways, and the development of PI3K isoform-selective inhibitors by both academic and pharmaceutical research has highlighted the importance of specific isoforms of PI3K in whole-animal physiology and pathology, e.g. PI3Kα in growth and metabolic regulation, PI3Kβ in thrombosis, and PI3Kδ and PI3Kγ in inflammation and asthma. Thus the Class I PI3K signalling pathway is emerging as an exciting new area for the development of novel therapeutics.

scholarly journals Monomeric C-reactive protein and Notch-3 co-operatively increase angiogenesis through PI3K signalling pathway

Cytokine ◽  
2014 ◽  
Vol 69 (2) ◽  
pp. 165-179 ◽  
Author(s):  
Emhamed Boras ◽  
Mark Slevin ◽  
M. Yvonne Alexander ◽  
Ali Aljohi ◽  
William Gilmore ◽  
...  
Keyword(s):  
Signalling Pathway ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Notch 3 ◽  
Pi3k Signalling

scholarly journals Oxypeucedanin hydrate monoacetate isolated from Angelica dahurica induces apoptosis in Caco-2 colon carcinoma cells through the mediation of PI3K-signalling pathway and inhibition of cancer cell migration

2016 ◽  
Vol 11 (2) ◽  
pp. 402 ◽  
Author(s):  
Yu Liu ◽  
Tian-Shu Peng ◽  
Xiang-Dang Hu ◽  
Shuai-Jun Li ◽  
Yong-Heng He ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Research Work ◽  
Signalling Pathway ◽  
Angelica Dahurica ◽  
Dependent Manner ◽  
Cancer Cell Migration ◽  
Cell Viability Assay ◽  
Pi3k Signalling

<p class="Abstract">The main aim of the present research work was to demonstrate the antitumor and apoptotic activities of oxypeucedanin hydrate monoacetate isolated from <em>Angelica dahurica</em> against Caco-2 colon cancer cells. MTT cell viability assay along with clonogenic assays were used to study the effect of the compound on cell cytotoxicity and the colony forming tendency. Fluorescence microscopy using acridine orange/ethidium bromide was used to study the effects on apoptosis. <em>In vitro</em> wound healing assay and Western blotting were carried out to study effect on cell migration and PI3K-signalling pathway. The results revealed that oxypeucedanin hydrate monoacetate inhibited Caco-2 cell proliferation and decreased the number of cancer colony forming cells. This compound exerted anti-migratory effects in dose- and time-dependent manner. As compared to the untreated control, drug-treated cells showed significant inhibition of cancer cell migration. Oxypeucedanin hydrate monoacetate significantly down-regulated the expression of pAkt and pPI3K in Caco-2 cells.</p><p> </p>

scholarly journals 300 GLUCOSAMINE SUPPLEMENTATION DURING IN VITRO MATURATION LEADS TO PERTURBED DEVELOPMENTAL CAPACITY OF BOVINE CUMULUS OOCYTE COMPLEXES

2005 ◽  
Vol 17 (2) ◽  
pp. 300 ◽  
Author(s):  
M. Sutton-McDowall ◽  
R. Gilchrist ◽  
J. Thompson
Keyword(s):  
Protein Synthesis ◽  
Follicular Fluid ◽  
Defined Medium ◽  
Signalling Pathway ◽  
Blastocyst Development ◽  
Fluid Medium ◽  
Nuclear Maturation ◽  
Developmental Capacity ◽  
Pi3k Signalling

Glucose is a primary energy substrate required for successful in vitro oocyte maturation (IVM). However, most maturation media contain more glucose than that seen in follicular fluid (2.3 mM vs. 5.6 mM in TCM199). Glucosamine (Glc) as an alternative substrate for extracellular matrix during cumulus expansion reduced glucose uptake by bovine cumulus oocyte complexes (COCs, Sutton-McDowall et al. 2004 Reproduction 128, 313–319). As this could enable a reduction in glucose concentrations to physiological levels in IVM medium of COCs, the aim of this study was to investigate the influence of Glc supplementation on oocyte developmental capacity. Bovine COCs were matured in synthetic follicular fluid medium (SFFM, a defined medium based on the composition of follicular fluid, plus 5.6 mM glucose, FSH, hCG and BSA, Sutton-McDowall et al. 2004 Reprod. Fertil. Dev. 16 sup, 204) ± 5 mM Glc. After 24 h, either nuclear maturation (rep = 8, n = 160) or blastocyst development 8 days post-fertilization (rep = 5, n = 400) was determined. Data was arcsine transformed and analyzed by ANOVA, followed by Tukey's test. While the presence of Glc did not affect the completion of nuclear maturation and early cleavage, +Glc led to severely perturbed blastocyst development (−Glc, 32.5 ± 1.9% vs. +Glc, 4.7 ± 3.9%, P < 0.001). Glc supplementation in somatic cells is well-known to down-regulate the phosphatidylinositol-3-kinase (PI3K) signalling pathway, reducing protein synthesis and other cell survival mechanisms. Therefore, oocyte protein synthesis (measured by [2,3,4,5,6-3H] phenylalanine incorporation, rep = 5, n = 200) and embryo development (rep = 6, n = 720) following IVM in SFFM ± Glc ± EGF (a PI3K pathway stimulator) was determined. Glc supplementation led to a 40% decrease in protein synthesis compared to −Glc, while the combination of +Glc + EGF significantly increased protein synthesis by 60%. However, IVM + EGF + Glc did not improve blastocyst rates (main effect: −Glc 41.6 ± 6.6% vs. +Glc, 6.6 ± 1.7%, P < 0.001). Additionally, COCs were also cultured in SFFM ± 50 μM LY294002 (a specific PI3K inhibitor) and nuclear maturation (rep = 5, n = 200) or blastocyst development 8 days post-fertilization (rep = 4, n = 200) was determined. Despite the presence of LY294002 leading to 43% less COCs completing nuclear maturation (P < 0.001), blastocyst development was not affected (mean = 38.8 ± 3.2%). These results demonstrate that Glc supplementation during IVM has no effect on nuclear maturation or early development but is detrimental to oocyte developmental capacity by severely perturbing blastocyst development. However, the diminished developmental capacity appears to be independent of the well-characterized Glc down-regulation of the PI3K signalling pathway. This work was supported by the Australian Research Council (SPIRT, C00107702) and Cook Australia Pty Ltd.

TCP1 Regulates PI3K/AKT/mTOR Signalling Pathway to Promote Ovarian Cancer Cell Proliferation

2020 ◽  
Author(s):  
Huixi Weng ◽  
Xiushan Feng ◽  
Yu Lan ◽  
Zhiqun Zheng
Keyword(s):  
Ovarian Cancer ◽  
Protein Expression ◽  
Western Blot ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Benign Ovarian Tumours ◽  
Pi3k Signalling

Abstract ObjectiveTCP1 is one of the eight subunits of the TCP1 ring complex (TRiC) or the multi-protein mammalian cytosolic chaperone complex. TRiC participates in protein folding and regulates the expression of multiple signalling proteins and cytoskeletal components in cells. Although the clinical importance of its subunits has been clarified in various carcinomas, the function of TCP1 in ovarian cancer (OC) remains unclear. We aimed to identify the association between the expression of TCP1 and epithelial ovarian cancer (EOC) development and patients’ prognosis, and explore the underlying mechanisms of TCP1 on the tumour progression of ovarian cancer cells.MethodsTCP1 protein expression was tested in the various ovarian tissues by immunohistochemistry (IHC), and the correlation between TCP1 expression and clinical physiologic or pathologic parameters of EOC patients was analyzed in this study. The relationship between TCP1 expression and ovarian cancer patients’ prognosis was collected and analyzed using the Kaplan-Meier (KM) Plotter online database. Then, the expression levels of TCP1 was tested in different OC cell lines by Western blot. Furthermore, a model using ovarian cancer cell line A2780 was constructed for studying the functions of TCP1 in human EOC cell growth, migration, and invasion. Finally, possible regulated signalling pathways were discussed.ResultsTCP1 protein expression in ovarian cancer or borderline tissue was significantly higher compared to that in benign ovarian tumours and normal ovarian tissue. The upregulated expression of TCP1 in ovarian cancer was positively associated with and the differentiation grade and FIGO stage, which predicted poor clinical outcomes. Compared with IOSE-80 cells, TCP1 protein was overexpressed in the A2780 cells. TCP1 knockdown using shRNA lentivirus inhibited cell viability in A2780 cells. Western blot showed that the phosphatidylinositol-3 kinase (PI3K) signalling pathway was activated in the tumour invasion of EOC driven by TCP1. ConclusionThe protein level of TCP1 is overexpressed in aggressive histologic types of epithelial ovarian cancer. Upregulated TCP1 is correlated with poor prognosis of patients and TCP1 may serve as a novel prognostic biomarker. The mechanism of cancer progression promoted by TCP1 upregulation may be linked to the PI3K signalling pathway activation and TCP1 may serve as a novel target for ovarian cancer treatment.

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