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Heydarigoojani Mahdieh - One of the best experts on this subject based on the ideXlab platform.

  • Thrombin receptor activating peptide-6 (TRAP-6) promotes human umbilical vein endothelial cells proliferation
    2019
    Co-Authors: Heydarigoojani Mahdieh
    Abstract:

    I. Abstract Objectives: Thrombin, a dominant coagulation protease has a vascularization-promoting function. Previous studies showed that the interaction between thrombin and human umbilical vein endothelial cell (HUVEC) results in upregulation in expression of vascular endothelial growth factors (VEGF) receptor. Thrombin signaling in endothelial cells mediated by protease-activated receptors (PARs). Thrombin cleaves the PAR-1, the predominant thrombin receptor in endothelial cells, and results in the tethered ligand; SFLLRN interacts with the extracellular loop of receptor and causes receptor activation. TRAP-6, a synthetic peptide that contains motif SFLLRN, showed agonist activity for thrombin. In this study, we investigated the effect of TRAP-6 on the proliferation of human umbilical vein endothelial cells and adipose-derived stem cells (ASCs). Furthermore, vasculogenesis function of TRAP-6 was determined on human umbilical vein endothelial cells/ adipose-derived stem cells co-culture. Moreover, the ability of TRAP-6 in stimulation of human umbilical vein endothelial cells to express various surface markers was determined. Approach and Results: Here, we used bromodeoxyuridine (BrdU) Assay to measure the proliferation of HUVEC and ASC. The results demonstrated that the proliferation of both HUVEC and ASC is enhanced. The HUVEC/ASC co-culture treated with TRAP-6 resulted in denser microvascular network formation in vitro and vascular network parameters such as the number of junctions, the number of tubules and total tubule length are enhanced. Furthermore, immunohistochemically investigation of surface markers in stimulated HUVEC with TRAP-6 using flow cytometry showed slightly increase of E-selectin, CD 73, thrombomodulin and CD 34 expression, decrease in CD 31 expression and no change in CD 146, VE-cadherin, Tie2, and VEGFR2 expression pattern. Conclusion: Our study provides detailed insight into angiogenetic behavior and influence of TRAP-6 on HUVECs. Our data demonstrate TRAP-6 improved either of HUVEC and ASC proliferation with no toxic effect. TRAP-induced HUVEC/ASC co-culture promotes microvascular network formation. However, the HUVEC surface markers do no indiacte significant change after stimulation with TRAP-6. Therefore, we concluded that TRAP-6 has potential in promoting angiogenesis and vascularization in tissue engineering.Mahdieh HeydarigoojaniZusammenfassung in deutscher SpracheTechnische Universität Wien, Diplomarbeit, 2019(VLID)448528

  • Thrombin receptor activating peptide-6 (TRAP-6) promotes human umbilical vein endothelial cells proliferation
    'Universidad Norbert Wiener', 2019
    Co-Authors: Heydarigoojani Mahdieh
    Abstract:

    I. Abstract Objectives: Thrombin, a dominant coagulation protease has a vascularization-promoting function. Previous studies showed that the interaction between thrombin and human umbilical vein endothelial cell (HUVEC) results in upregulation in expression of vascular endothelial growth factors (VEGF) receptor. Thrombin signaling in endothelial cells mediated by protease-activated receptors (PARs). Thrombin cleaves the PAR-1, the predominant thrombin receptor in endothelial cells, and results in the tethered ligand; SFLLRN interacts with the extracellular loop of receptor and causes receptor activation. TRAP-6, a synthetic peptide that contains motif SFLLRN, showed agonist activity for thrombin. In this study, we investigated the effect of TRAP-6 on the proliferation of human umbilical vein endothelial cells and adipose-derived stem cells (ASCs). Furthermore, vasculogenesis function of TRAP-6 was determined on human umbilical vein endothelial cells/ adipose-derived stem cells co-culture. Moreover, the ability of TRAP-6 in stimulation of human umbilical vein endothelial cells to express various surface markers was determined. Approach and Results: Here, we used bromodeoxyuridine (BrdU) Assay to measure the proliferation of HUVEC and ASC. The results demonstrated that the proliferation of both HUVEC and ASC is enhanced. The HUVEC/ASC co-culture treated with TRAP-6 resulted in denser microvascular network formation in vitro and vascular network parameters such as the number of junctions, the number of tubules and total tubule length are enhanced. Furthermore, immunohistochemically investigation of surface markers in stimulated HUVEC with TRAP-6 using flow cytometry showed slightly increase of E-selectin, CD 73, thrombomodulin and CD 34 expression, decrease in CD 31 expression and no change in CD 146, VE-cadherin, Tie2, and VEGFR2 expression pattern. Conclusion: Our study provides detailed insight into angiogenetic behavior and influence of TRAP-6 on HUVECs. Our data demonstrate TRAP-6 improved either of HUVEC and ASC proliferation with no toxic effect. TRAP-induced HUVEC/ASC co-culture promotes microvascular network formation. However, the HUVEC surface markers do no indiacte significant change after stimulation with TRAP-6. Therefore, we concluded that TRAP-6 has potential in promoting angiogenesis and vascularization in tissue engineering.5

Faranak Fallahian - One of the best experts on this subject based on the ideXlab platform.

  • adenosine induces cell cycle arrest and apoptosis in androgen dependent and independent prostate cancer cell lines lncap fgc 10 du 145 and pc3
    The Prostate, 2012
    Co-Authors: Mahmoud Aghaei, Fatemeh Karamitehrani, Mojtaba Panjehpour, Siamak Salami, Faranak Fallahian
    Abstract:

    BACKGROUND Adenosine has been shown to inhibit cell growth and induce apoptosis in the several cancer cells via intrinsic and extrinsic pathway. The present study was designed to understand the mechanism underlying adenosine-induced apoptosis in the DU-145, PC3, and LNcap-FGC10 human prostate cancer cells. METHODS To observe cell viability and proliferation, MTT Assay, cell counting, and BrdU Assay were carried out in DU-145, PC3, and LNcap-FGC10 cells. Apoptosis was assessed with the analysis of cell cycle, Hoechst 33258 staining, propidium iodide and annexin-V staining, reactive oxygen species (ROS) formation, mitochondrial membrane potential (ΔΨM) measurement, caspase-3 activity Assay, Bcl-2 and Bax protein expression. Moreover, the expression of adenosine receptors and the effects of adenosine receptor (A1, A2a, and A3) antagonists were examined. RESULT Adenosine significantly reduced cell proliferation in a dose-dependent manner in DU-145, PC3, and LNcap-FGC10 cell lines. Adenosine induced arrest in the cell-cycle progression in G0/G1 phase through Cdk4/cyclinD1-mediated pathway. Adenosine induced apoptosis, which was determined by morphological changes and increased sub-G1 population. Furthermore, increase of ROS, loss of MMP, activation of caspase-3, and down-regulation of Bcl-2 expression was observed. A1, A2a, A2b, and A3 adenosine receptors mRNA are expressed in the cell lines. Moreover, adenosine-induced apoptosis was inhibited by MRS1220, A3 adenosine receptor antagonist. CONCLUSION Our results suggest that adenosine induced apoptosis in prostate cancer cells via the mitochondrial pathway and is related to the adenosine receptors. These data might suggest that adenosine could be used as an agent for the treatment of prostate cancer. Prostate 72:361–375, 2012. © 2011 Wiley Periodicals, Inc.

  • adenosine induces cell cycle arrest and apoptosis in androgen dependent and independent prostate cancer cell lines lncap fgc 10 du 145 and pc3
    The Prostate, 2012
    Co-Authors: Mahmoud Aghaei, Fatemeh Karamitehrani, Mojtaba Panjehpour, Siamak Salami, Faranak Fallahian
    Abstract:

    BACKGROUND Adenosine has been shown to inhibit cell growth and induce apoptosis in the several cancer cells via intrinsic and extrinsic pathway. The present study was designed to understand the mechanism underlying adenosine-induced apoptosis in the DU-145, PC3, and LNcap-FGC10 human prostate cancer cells. METHODS To observe cell viability and proliferation, MTT Assay, cell counting, and BrdU Assay were carried out in DU-145, PC3, and LNcap-FGC10 cells. Apoptosis was assessed with the analysis of cell cycle, Hoechst 33258 staining, propidium iodide and annexin-V staining, reactive oxygen species (ROS) formation, mitochondrial membrane potential (ΔΨM) measurement, caspase-3 activity Assay, Bcl-2 and Bax protein expression. Moreover, the expression of adenosine receptors and the effects of adenosine receptor (A1, A2a, and A3) antagonists were examined. RESULT Adenosine significantly reduced cell proliferation in a dose-dependent manner in DU-145, PC3, and LNcap-FGC10 cell lines. Adenosine induced arrest in the cell-cycle progression in G0/G1 phase through Cdk4/cyclinD1-mediated pathway. Adenosine induced apoptosis, which was determined by morphological changes and increased sub-G1 population. Furthermore, increase of ROS, loss of MMP, activation of caspase-3, and down-regulation of Bcl-2 expression was observed. A1, A2a, A2b, and A3 adenosine receptors mRNA are expressed in the cell lines. Moreover, adenosine-induced apoptosis was inhibited by MRS1220, A3 adenosine receptor antagonist. CONCLUSION Our results suggest that adenosine induced apoptosis in prostate cancer cells via the mitochondrial pathway and is related to the adenosine receptors. These data might suggest that adenosine could be used as an agent for the treatment of prostate cancer. Prostate 72:361–375, 2012. © 2011 Wiley Periodicals, Inc.

Ivana Novak - One of the best experts on this subject based on the ideXlab platform.

  • the p2x7 receptor regulates cell survival migration and invasion of pancreatic ductal adenocarcinoma cells
    Molecular Cancer, 2015
    Co-Authors: Andrea Giannuzzo, Stine F Pedersen, Ivana Novak
    Abstract:

    Pancreatic ductal adenocarcinoma (PDAC) is presently one of the cancers with the worst survival rates and least effective treatments. Moreover, total deaths due to PDAC are predicted to increase in the next 15 years. Therefore, novel insights into basic mechanism of PDAC development and therapies are needed. PDAC is characterized by a complex microenvironment, in which cancer and stromal cells release different molecules, such as ATP. ATP can be transported and/or exocytosed from active cancer cells and released from dying cells in the necrotic core of the cancer. We hypothesized that one of the ATP receptors, the P2X7 receptor (P2X7R) could be an important player in PDAC behaviour. We determined the expression (real time PCR and Western blot) and localization (immunofluorescence) of P2X7R in human PDAC cell lines (AsPC-1, BxPC-3, Capan-1, MiaPaCa-2, Panc-1) and a “normal” human pancreatic duct epithelial cell line (HPDE). The function of P2X7R in proliferation (BrdU Assay), migration (wound Assay) and invasion (Boyden chamber with matrigel) was characterized. Furthermore, we studied P2X7R-dependent pore formation (YoPro-1 Assay) and cell death (caspase and annexin V / propidium iodide Assays). We found higher expression of P2X7R protein in PDAC compared to HPDE cells. P2X7R had notable disparate effects on PDAC survival. Firstly, high concentrations of ATP or the specific P2X7R agonist, BzATP, had cytotoxic effects in all cell lines, and cell death was mediated by necrosis. Moreover, the P2X7R–pore antagonist, A438079, prevented ATP-induced pore formation and cell death. Second, in basal conditions and with low concentrations of ATP/BzATP, the P2X7R allosteric inhibitor AZ10606120 reduced proliferation in all PDAC cell lines. P2X7R also affected other key characteristics of cancer cell behavior. AZ10606120 reduced cell migration and invasion in PDAC cell lines compared to that of untreated/vehicle-treated control cells, and stimulation with sub-millimolar concentrations of ATP or BzATP substantially increased cell invasion. PDAC cell lines overexpress P2X7R and the receptor plays crucial roles in cell survival, migration and invasion. Therefore, we propose that drugs targeting P2X7R could be exploited in therapy of pancreatic cancer.

Hong Wang - One of the best experts on this subject based on the ideXlab platform.

  • hoxa5 inhibits the proliferation and induces the apoptosis of cervical cancer cells via regulation of protein kinase b and p27
    Oncology Reports, 2018
    Co-Authors: Zefei Wang, Hong Wang
    Abstract:

    Homeobox A5 (HOXA5) is a member of the homeobox gene (HOX) family, which plays an important role in the development of various malignant tumors. Here, we speculated that HOXA5 has an effect on cervical cancer development. In our study, we aimed to explore the role and molecular mechanism of HOXA5 in regards to the cell proliferation and apoptosis in cervical cancer. We found that expression levels of HOXA5 measured by RT‑qPCR and western blot Assays in cervical cancer cell lines and tissues were both significantly downregulated. We performed a gain‑of‑function experiment by the transfection with pcDNA.3.1‑HOXA5 in ME‑180 and HT‑3 cells to overexpress HOXA5, and the caspase‑3 activity measured by caspase‑3 activity Assay kit and cell apoptosis detected by flow cytometry were obviously promoted. Meanwhile, cell proliferation tested by BrdU Assay, invasion determined by Transwell and cell viability tested by MTT were inhibited. Moreover, protein kinase B (AKT) was activated by incubation with SC79 (AKT activator; 1 µg/ml) after HOXA5 overexpression, and reversed the effect of HOXA5 overexpression on p27 expression. Additionally, significant elevation of AKT activation measured by western blot analysis abrogated the effect of HOXA5 on caspase‑3 activity, cell apoptosis, proliferation, invasion and cell viability. Taken together, this study revealed that HOXA5 inhibits cervical cancer progression by regulating AKT/p27, proposing the potential role of HOXA5 in the prevention and treatment of cervical cancer.

Tang Sheng-jian - One of the best experts on this subject based on the ideXlab platform.

  • FOXL2 suppresses proliferation, invasion and promotes apoptosis of cervical cancer cells
    international journal of clinical and experimental pathology, 2014
    Co-Authors: Liu Xing-long, Meng Yu-han, Wang Jian-li, Yang Biao-bing, Zhang Fan, Tang Sheng-jian
    Abstract:

    FOXL2 is a transcription factor that is essential for ovarian function and maintenance, the germline mutations of which give rise to the blepharophimosis ptosis epicanthus inversus syndrome (BPES), often associated with premature ovarian failure. Recently, its mutations have been found in ovarian granulosa cell tumors (OGCTs). In this study, we measured the expression of FOXL2 in cervical cancer by immunohistochemistry and its mRNA level in cervical cancer cell lines Hela and Siha by RT-PCR. Then we overexpressed FOXL2 in Hela cells and silenced it in Siha cells by plasmid transfection and verified using western blotting. When FOXL2 was overexpressed or silenced, cells proliferation and apoptosis were determined by BrdU Assay and Annexin V/PI detection kit, respectively. In addition, we investigated the effects of FOXL2 on the adhesion and invasion of Hela and Siha cells. Finally, we analyzed the influences of FOXL2 on Ki67, PCNA and FasL by flow cytometry. The results showed that FOXL2 was highly expressed in cervical squamous cancer. Overexpressing FOXL2 suppressed Hela proliferation and facilitated its apoptosis. Silencing FOXL2 enhanced Siha proliferation and inhibited its apoptosis. Meanwhile, silencing FOXL2 promoted Siha invasion, but it had no effect on cells adhesion. In addition, overexpressing FOXL2 decreased the expression of Ki67 in Hela and Siha cells. Therefore, our results suggested that FOXL2 restrained cells proliferation and enhanced cells apoptosis mainly through decreasing Ki67 expression.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000335227600026&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701OncologyPathologySCI(E)PubMed2ARTICLEtsj3676@126.com41534-1543