scholarly journals Role of Angiopoietin-2 in Regulating Growth and Vascularity of Astrocytomas

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Gelareh Zadeh ◽  
Keyvan Koushan ◽  
Qian Baoping ◽  
Patrick Shannon ◽  
Abhijit Guha
Keyword(s):  
Tumor Angiogenesis ◽  
Cancer Biology ◽  
Critical Role ◽  
Tumor Stage ◽  
Growth Stages ◽  
Vascular Growth ◽  
Malignant Astrocytomas ◽  
Significant Research ◽  
Angiopoietin 2

Angiopoietins and Tie2 are angiogenic-specific ligand and receptor complex that have been shown to play a critical role in tumor angiogenesis. Angiopoietin-2 (Ang2) is one of four ligands for receptor Tie2 and it is the naturally occurring antagonist to Tie2, inhibiting the action of Angiopoietin-1 (Ang1). Over the last decade, significant research has focused on elucidating the role of Ang2 in cancer biology and its exact role in tumor angiogenesis remains elusive. In this study we have focused on establishing the role of Ang2 in angiogenesis of malignant astrocytomas. We have demonstrated that Ang2 significantly enhances the vascular growth of malignant astrocytomas and constant upregulation of Ang2 throughout all phases of tumor growth generates abnormal vascular structures that are not typically seen in human astrocytomas, suggesting that Ang2 plays a tumor stage-dependent role and is not a consistently elevated throughout all growth stages of malignant astroctyomas.

Impact and mechanistic role of MicroRNA-1291 on pancreatic tumorigenesis.

2016 ◽  
Vol 34 (4_suppl) ◽  
pp. 243-243 ◽  
Author(s):  
Mei-Juan Tu ◽  
Yu-Zhuo Pan ◽  
Jing-Xin Qiu ◽  
Edward Jae-hoon Kim ◽  
Aiming Yu
Keyword(s):  
Cell Cycle ◽  
Cancer Biology ◽  
Critical Role ◽  
Experimental Studies ◽  
Mass Spectrometry Analysis ◽  
Ductal Adenocarcinoma ◽  
Luciferase Reporter ◽  
Spectrometry Analysis

243 Background: Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer death. Better understanding of pancreatic cancer biology and identification of new targets are highly warranted. MicroRNAs (miRs or miRNAs) play a critical role in the control of tumor progression via crosstalk with cancer signaling pathways. Our recent studies showed that miR-1291 improved chemosensitivity through targeting of efflux transporter ABCC1. This current study investigated the mechanistic role of miR-1291 in the suppression of pancreatic tumorigenesis. Methods: PANC-1 and AsPC-1 cell lines were stably transfected with miR-1291. Cell cycle status and apoptosis of stable miR-1291-expressing cells were tested against control cells using flow cytometry. Cells were injected subcutaneously into nude mice and tumorigenesis was measured in vivo. Proteomic studies were performed by two-dimensional difference gel electrophoresis, matrix-assisted laser desorption/ionization time of flight mass spectrometry analysis. Computationally predicted miR-1291 targets were assessed by luciferase reporter assay and Western blot. Primary PDAC and control samples were tested for miR-1291 and target gene expression levels. Results: Our data showed that stable miR-1291-expressing PANC-1 and AsPC-1 cells both showed a significantly lower rate of proliferation than the control cells, which was associated with a cell cycle arrest and enhanced apoptosis. Furthermore, miR-1291 suppressed the tumorigenesis of PANC-1 cells in mouse models in vivo. Proteomic studies revealed the protein level of several cancer-related genes were downregulated by miR-1291, including a pancreatic tumor promoting protein AGR2 which was reduced ~10-fold. Through computational and experimental studies we further identified that FOXA2, a transcription factor governing AGR2 expression, was a direct target of miR-1291. In addition, we found a significant down-regulation of miR-1291 in a set of PDAC patient tumor samples overexpressing AGR2. Conclusions: These results indicate that miR-1291 suppresses pancreatic tumorigenesis via targeting of FOXA2-AGR regulatory pathway providing new insight supporting development of miR-1291-based therapy for PDAC.

scholarly journals Myeloid Cells in the Tumor Microenvironment: Modulation of Tumor Angiogenesis and Tumor Inflammation

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Michael C. Schmid ◽  
Judith A. Varner
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Angiogenesis ◽  
Malignant Tumors ◽  
Critical Role ◽  
Myeloid Cells ◽  
Suppressor Cells ◽  
Myeloid Cell ◽  
Promote Tumor Growth ◽  
Bone Marrow Derived Cells

Myeloid cells are a heterogeneous population of bone marrow-derived cells that play a critical role during growth and metastasis of malignant tumors. Tumors exhibit significant myeloid cell infiltrates, which are actively recruited to the tumor microenvironment. Myeloid cells promote tumor growth by stimulating tumor angiogenesis, suppressing tumor immunity, and promoting metastasis to distinct sites. In this review, we discuss the role of myeloid cells in promoting tumor angiogenesis. Furthermore, we describe a subset of myeloid cells with immunosuppressive activity (known as myeloid-derived suppressor cells). Finally, we will comment on the mechanisms regulating myeloid cell recruitment to the tumor microenvironment and on the potential of myeloid cells as new targets for cancer therapy.

On the uniqueness of, and diversity within, cancers: A commentary on Kangas and Gross 2018

2018 ◽  
Vol 25 (1) ◽  
pp. 26-30
Author(s):  
Wolfgang Linden ◽  
Andrea Vodermaier
Keyword(s):  
Gender Differences ◽  
Cancer Care ◽  
Critical Role ◽  
Tumor Stage ◽  
Phase Model ◽  
Fear Of Recurrence ◽  
Coping Process ◽  
Emotion Coping ◽  
And Gender

This commentary accompanies publication of Kangas and Gross’ phase model of emotion coping throughout the process of cancer care. While supporting the model, this commentary additionally highlights the already existing knowledge about the critical role of tumor stage, patient age, uncertainty and fear of recurrence, and gender differences. It is briefly described how all of these factors moderate and mediate the emotion coping process.

MEKK3 is required for endothelium function but is not essential for tumor growth and angiogenesis

2007 ◽  
Vol 293 (4) ◽  
pp. C1404-C1411 ◽  
Author(s):  
Yong Deng ◽  
Jianhua Yang ◽  
Marya McCarty ◽  
Bing Su
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Tumor Growth ◽  
Tumor Angiogenesis ◽  
Critical Role ◽  
Embryonic Stem ◽  
Angiogenic Factor ◽  
Endothelial Cell Proliferation ◽  
Wild Type

Mitogen-activated protein kinase kinase kinase 3 (MEKK3) plays an essential role in embryonic angiogenesis, but its role in tumor growth and angiogenesis is unknown. In this study, we further investigated the role of MEKK3 in embryonic angiogenesis, tumor angiogenesis, and angiogenic factor production. We found that endothelial cells from Mekk3-deficient embryos showed defects in cell proliferation, apoptosis, and interactions with myocardium in the heart. We also found that MEKK3 is required for angiopoietin-1 (Ang1)-induced p38 and ERK5 activation. To study the role of MEKK3 in tumor growth and angiogenesis, we established both wild-type and Mekk3-deficient tumor-like embryonic stem cell lines and transplanted them subcutaneously into nude mice to assess their ability to grow and induce tumor angiogenesis. Mekk3-deficient tumors developed and grew similarly as control Mekk3 wild-type tumors and were also capable of inducing tumor angiogenesis. In addition, we found no differences in the production of VEGF in Mekk3-deficient tumors or embryos. Taken together, our results suggest that MEKK3 plays a critical role in Ang1/Tie2 signaling to control endothelial cell proliferation and survival and is required for endothelial cells to interact with the myocardium during early embryonic development. However, MEKK3 is not essential for tumor growth and angiogenesis.

scholarly journals Cell proliferation depends on the direct binding between PKM2 and AKAP-Lbc

2017 ◽  
Author(s):  
Xinping Chen ◽  
Graeme K. Carnegie
Keyword(s):  
Cell Proliferation ◽  
Cancer Biology ◽  
Critical Role ◽  
Glycolytic Enzyme ◽  
Bimolecular Fluorescence Complementation ◽  
Amino Acid Residues ◽  
Anchoring Protein ◽  
Blast Cells ◽  
Direct Binding

AbstractThe M2 form of the glycolytic enzyme pyruvate kinase (PKM2) has generated much interest recently due to its important role in tumor metabolism. A yeast two-hybrid screen carried out by the Alliance for Cell Signaling suggests that PKM2 interacts with A-Kinase Anchoring Protein (AKAP)-Lbc.AKAP-Lbc (also known as AKAP13) is a scaffold protein that integrates signaling through multiple enzymes including protein kinases A and D and the small G protein Rho. AKAP-Lbc was originally identified in leukemic blast cells, and multiple reports implicate AKAP-Lbc in breast, prostate and thyroid cancers, however the role of AKAP-Lbc in cancer biology is not understood.Co-immunoprecipitation, pulldown and Bimolecular Fluorescence Complementation (BiFC) data indicate that PKM2 interacts with AKAP-Lbc. Mapping experiments indicate that PKM2 directly interacts with amino acid residues 1923-2817 of AKAP-Lbc. By disrupting the interaction between the two proteins with the expression of the AKAP-Lbc fragments, our data suggest that the binding between PKM2 and PKA plays a critical role in cell proliferation. The work indicates that the binding between AKAP-Lbc and PKM2 may be an important target to treat some cancers by reducing the cell proliferation.

scholarly journals The mini player with diverse functions: extracellular vesicles in cell biology, disease, and therapeutics

2021 ◽  
Author(s):  
Abhimanyu Thakur ◽  
Xiaoshan Ke ◽  
Ya-Wen Chen ◽  
Pedram Motallebnejad ◽  
Kui Zhang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Cell Biology ◽  
Cancer Biology ◽  
Cell Types ◽  
Research Progress ◽  
Drug Delivery Vehicles ◽  
Significant Research

AbstractExtracellular vesicles (EVs) are tiny biological nanovesicles ranging from approximately 30–1000 nm in diameter that are released into the extracellular matrix of most cell types and in biofluids. The classification of EVs includes exosomes, microvesicles, and apoptotic bodies, dependent on various factors such as size, markers, and biogenesis pathways. The transition of EV relevance from that of being assumed as a trash bag to be a key player in critical physiological and pathological conditions has been revolutionary in many ways. EVs have been recently revealed to play a crucial role in stem cell biology and cancer progression via intercellular communication, contributing to organ development and the progression of cancer. This review focuses on the significant research progress made so far in the role of the crosstalk between EVs and stem cells and their niche, and cellular communication among different germ layers in developmental biology. In addition, it discusses the role of EVs in cancer progression and their application as therapeutic agents or drug delivery vehicles. All such discoveries have been facilitated by tremendous technological advancements in EV-associated research, especially the microfluidics systems. Their pros and cons in the context of characterization of EVs are also extensively discussed in this review. This review also deliberates the role of EVs in normal cell processes and disease conditions, and their application as a diagnostic and therapeutic tool. Finally, we propose future perspectives for EV-related research in stem cell and cancer biology.

scholarly journals Role of Kisspeptin in Female Infertility

Pulse ◽  
2016 ◽  
Vol 8 (1) ◽  
pp. 43-50
Author(s):  
Md Rafiqul Islam Bhuiyan ◽  
SM Khaliduzzaman ◽  
Khairun Nahar Priti
Keyword(s):  
Cancer Biology ◽  
Tumor Metastasis ◽  
Critical Role ◽  
Animal Data ◽  
Human Reproductive ◽  
Puberty Onset ◽  
Inactivating Mutation ◽  
G Protein Coupled ◽  
Gpr54 Gene

Background: Kiss1, a noble G protein coupled receptor designated as GPR54, was first identified in rat brain in 1999 and orthologue gene identified in human in 2001 the original niche for the function of kisspeptin was restricted to cancer biology for their ability to suppress tumor metastasis. However, kisspeptin has recently emerged as a key player in the field of reproductive endocrinology.Method: A systematic literature review was done by using PUBMED. Though there is lack of human data, used animal data also hold translational potential for human. Results: Inactivating mutation of GPR54 gene is linked with absence of puberty onset and idiopathic hypogonadotrophic hypogonadism. Furthermore, recent studies support critical role of kisspeptin/GPR54 system on regulation of GnRH neurons, involvement of puberty onset and gonadal steroid feedback.Conclusion: This review will briefly discuss on cellular and molecular level of kisspeptin, their potential effects on human and clinical application of kisspeptin on human reproductive disorder.Pulse Vol.8 January-December 2015 p.43-50

Phytomers, phyllochrons, phenology and temperate cereal development

2005 ◽  
Vol 143 (2-3) ◽  
pp. 137-150 ◽  
Author(s):  
G S. McMASTER
Keyword(s):  
Abiotic Factors ◽  
Spring Barley ◽  
Critical Role ◽  
Agricultural Science ◽  
Growth Stages ◽  
Leaf Appearance ◽  
Temperate Cereal ◽  
Rate Of Leaf Appearance ◽  
Key Questions

Extensive research has been conducted on temperate cereal development since the inception of the Journal of Agricultural Science, Cambridge in 1905. This review presents an overview of the orderly and predictable development of wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.). It begins with the concept of building canopies by the formation, growth and senescence of phytomers (the unit comprised of the leaf, axillary bud, node and internode). Morphological naming schemes for uniquely identifying each plant part are then extended to uniquely name each phytomer unit. The role of the phyllochron (rate of leaf appearance) in synchronizing cereal development and phytomer formation is discussed, as is the use of phenology to predict the timing of the formation, growth and senescence of individual components. The complete developmental sequence of the winter wheat shoot apex correlated with growth stages is extended to spring barley. This overview discusses the abiotic factors controlling cereal development, with special attention given to key questions regarding the critical role of temperature. The review concludes with some cautious glances forward to the exciting possibilities for better understanding of mechanisms controlling the phyllochron and phenology being gained from advances in functional genomics and molecular biology.

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