scholarly journals Undervalued ubiquitous proteins

4open ◽  
2019 ◽  
Vol 2 ◽  
pp. 7 ◽  
Author(s):  
Björn L.D.M. Brücher ◽  
Ijaz S. Jamall
Keyword(s):  
Cancer Progression ◽  
Cancer Biology ◽  
Life Forms ◽  
Intercellular Signaling ◽  
Peptide Bonds ◽  
True Nature ◽  
The Stability ◽  
Quantitative Contribution ◽  
Ubiquitous Proteins

The role of ubiquitous proteins (UPs) and their corresponding enzymes have been underestimated in carcinogenesis as the focus of much research revolved around measuring mutations and/or other genetic epiphenomena as surrogate markers of cancer and cancer progression. Over the past three decades, the scientific community has come to realize that the concentration on microdissection of cancer cells without accounting for the neighborhood in which these cells reside, i.e., the stroma, fails to reflect the true nature of cancer biology. UPs are fundamental for cellular homeostasis and phylogenetic development as well as for the integrity of the cytoskeleton and for the stability of cells and tissues in regards to intercellular signaling, cell shape and mobility, apoptosis, wound healing, and cell polarity. Corresponding enzymes are used by microorganisms to gain entry into the host by degradation of UPs and play a role to cleave peptide bonds for killing disease-causing life forms along for the creation of the precancerous niche (PCN) during carcinogenesis, cancer invasion, and in metastasis. The language used by such proteins as well as their complementary enzymes with its influence on multiple pathways and the cross-linked extracellular matrix is incompletely understood. The role of UPs in the disruption of signaling homeostasis and resulting interference with crosstalk in carcinogenesis appears sufficiently delineated to warrant a much more refined examination of their qualitative and quantitative contribution to the development of cancer and cancer therapy.

scholarly journals Biological mechanisms linked to inflammation in cancer: Discovery of tumor microenvironment-related biomarkers and their clinical application in solid tumors

2020 ◽  
Vol 35 (1_suppl) ◽  
pp. 8-11 ◽  
Author(s):  
Paola Nisticò ◽  
Gennaro Ciliberto
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Tumor Development ◽  
Short Paper ◽  
Great Relevance ◽  
Cellular Components ◽  
The Relationship

Our view of cancer biology radically shifted from a “cancer-cell-centric” vision to a view of cancer as an organ disease. The concept that genetic and/or epigenetic alterations, at the basis of cancerogenesis, are the main if not the exclusive drivers of cancer development and the principal targets of therapy, has now evolved to include the tumor microenvironment in which tumor cells can grow, proliferate, survive, and metastasize only within a favorable environment. The interplay between cancer cells and the non-cellular and cellular components of the tumor microenvironment plays a fundamental role in tumor development and evolution both at the primary site and at the level of metastasis. The shape of the tumor cells and tumor mass is the resultant of several contrasting forces either pro-tumoral or anti-tumoral which have at the level of the tumor microenvironment their battle field. This crucial role of tumor microenvironment composition in cancer progression also dictates whether immunotherapy with immune checkpoint inhibitor antibodies is going to be efficacious. Hence, tumor microenvironment deconvolution has become of great relevance in order to identify biomarkers predictive of efficacy of immunotherapy. In this short paper we will briefly review the relationship between inflammation and cancer, and will summarize in 10 short points the key concepts learned so far and the open challenges to be solved.

scholarly journals Genetic and Epigenetic Events Generate Multiple Pathways in Colorectal Cancer Progression

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Massimo Pancione ◽  
Andrea Remo ◽  
Vittorio Colantuoni
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Current Knowledge ◽  
Alternative Pathway ◽  
Epigenetic Events ◽  
Cells Of Origin ◽  
Common Causes ◽  
Colorectal Cancer Progression

Colorectal cancer (CRC) is one of the most common causes of death, despite decades of research. Initially considered as a disease due to genetic mutations, it is now viewed as a complex malignancy because of the involvement of epigenetic abnormalities. A functional equivalence between genetic and epigenetic mechanisms has been suggested in CRC initiation and progression. A hallmark of CRC is its pathogenetic heterogeneity attained through at least three distinct pathways: a traditional (adenoma-carcinoma sequence), an alternative, and more recently the so-called serrated pathway. While the alternative pathway is more heterogeneous and less characterized, the traditional and serrated pathways appear to be more homogeneous and clearly distinct. One unsolved question in colon cancer biology concerns the cells of origin and from which crypt compartment the different pathways originate. Based on molecular and pathological evidences, we propose that the traditional and serrated pathways originate from different crypt compartments explaining their genetic/epigenetic and clinicopathological differences. In this paper, we will discuss the current knowledge of CRC pathogenesis and, specifically, summarize the role of genetic/epigenetic changes in the origin and progression of the multiple CRC pathways. Elucidation of the link between the molecular and clinico-pathological aspects of CRC would improve our understanding of its etiology and impact both prevention and treatment.

scholarly journals The Role of Cysteine Cathepsins in Cancer Progression and Drug Resistance

2019 ◽  
Vol 20 (14) ◽  
pp. 3602 ◽  
Author(s):  
Magdalena Rudzińska ◽  
Alessandro Parodi ◽  
Surinder M. Soond ◽  
Andrey Z. Vinarov ◽  
Dmitry O. Korolev ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Lysosomal Enzymes ◽  
Tumor Biology ◽  
Therapeutic Strategies ◽  
Cysteine Cathepsins ◽  
Aggressive Tumor ◽  
Tumor Phenotypes

Cysteine cathepsins are lysosomal enzymes belonging to the papain family. Their expression is misregulated in a wide variety of tumors, and ample data prove their involvement in cancer progression, angiogenesis, metastasis, and in the occurrence of drug resistance. However, while their overexpression is usually associated with highly aggressive tumor phenotypes, their mechanistic role in cancer progression is still to be determined to develop new therapeutic strategies. In this review, we highlight the literature related to the role of the cysteine cathepsins in cancer biology, with particular emphasis on their input into tumor biology.

scholarly journals Role of Phage Capsid in the Resistance to UV-C Radiations

2021 ◽  
Vol 22 (7) ◽  
pp. 3408
Author(s):  
Laura Maria De Plano ◽  
Domenico Franco ◽  
Maria Giovanna Rizzo ◽  
Vincenzo Zammuto ◽  
Concetta Gugliandolo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
3D Modelling ◽  
Wild Type ◽  
Peptide Bonds ◽  
Environmental Resistance ◽  
Modelling Analysis ◽  
Phage Capsid ◽  
The Stability ◽  
Uv C

The conformational variation of the viral capsid structure plays an essential role both for the environmental resistance and acid nuclear release during cellular infection. The aim of this study was to evaluate how capsid rearrangement in engineered phages of M13 protects viral DNA and peptide bonds from damage induced by UV-C radiation. From in silico 3D modelling analysis, two M13 engineered phage clones, namely P9b and 12III1, were chosen for (i) chemical features of amino acids sequences, (ii) rearrangements in the secondary structure of their pVIII proteins and (iii) in turn the interactions involved in phage capsid. Then, their resistance to UV-C radiation and hydrogen peroxide (H2O2) was compared to M13 wild-type vector (pC89) without peptide insert. Results showed that both the phage clones acquired an advantage against direct radiation damage, due to a reorganization of interactions in the capsid for an increase of H-bond and steric interactions. However, only P9b had an increase in resistance against H2O2. These results could help to understand the molecular mechanisms involved in the stability of new virus variants, also providing quick and necessary information to develop effective protocols in the virus inactivation for human activities, such as safety foods and animal-derived materials.

scholarly journals Communication Between Epithelial–Mesenchymal Plasticity and Cancer Stem Cells: New Insights Into Cancer Progression

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaobo Zheng ◽  
Fuzhen Dai ◽  
Lei Feng ◽  
Hong Zou ◽  
Li Feng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Epithelial Mesenchymal Transition ◽  
Current Knowledge ◽  
Mesenchymal Transition ◽  
Binary Model ◽  
Epithelial Phenotype

The epithelial–mesenchymal transition (EMT) is closely associated with the acquisition of aggressive traits by carcinoma cells and is considered responsible for metastasis, relapse, and chemoresistance. Molecular links between the EMT and cancer stem cells (CSCs) have indicated that EMT processes play important roles in the expression of CSC-like properties. It is generally thought that EMT-related transcription factors (EMT-TFs) need to be downregulated to confer an epithelial phenotype to mesenchymal cells and increase cell proliferation, thereby promoting metastasis formation. However, the genetic and epigenetic mechanisms that regulate EMT and CSC activation are contradictory. Emerging evidence suggests that EMT need not be a binary model and instead a hybrid epithelial/mesenchymal state. This dynamic process correlates with epithelial–mesenchymal plasticity, which indicates a contradictory role of EMT during cancer progression. Recent studies have linked the epithelial–mesenchymal plasticity and stem cell-like traits, providing new insights into the conflicting relationship between EMT and CSCs. In this review, we examine the current knowledge about the interplay between epithelial–mesenchymal plasticity and CSCs in cancer biology and evaluate the controversies and future perspectives. Understanding the biology of epithelial–mesenchymal plasticity and CSCs and their implications in therapeutic treatment may provide new opportunities for targeted intervention.

Role of Organ Specific Cancer Stem Cells in Organ Specific Cancer Progression

2020 ◽  
Vol 6 (2) ◽  
pp. 21
Author(s):  
Muhammad Ali ◽  
Fatima Ali ◽  
Nadia Wajid
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Cancer Therapeutics ◽  
Therapeutic Approaches ◽  
Specific Cancer ◽  
Organ Specific

Since the cancer stem cells (CSC) have been identified in 1997 by Bonnet and Dick, more than 100,000 papers have been published on the CSC. Huge research on cancer stem cells helped the scientists to rethink about the cancer therapeutics as classic way of chemotherapy is ineffective because chemotherapy failed to kill these cells, the only reason of cancer relapse. The cancer theory of stem cells is one of the most trending theory in stem cells and cancer biology focusing on the understanding of biology of cancer cells for an enhanced and improved therapeutic approaches should be applied to cure the cancer. This mini-review is a short overview on the role of organ specific cancer stem cells in the organ specific cancer progression.

scholarly journals The Cancer Clock Is (Not) Ticking: Links between Circadian Rhythms and Cancer

2019 ◽  
Vol 1 (4) ◽  
pp. 435-458 ◽  
Author(s):  
Monica N. Morgan ◽  
Sapir Dvuchbabny ◽  
Chloe-Anne Martinez ◽  
Bernadette Kerr ◽  
Peter A. Cistulli ◽  
...  
Keyword(s):  
Cell Division ◽  
Circadian Rhythms ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Environmental Changes ◽  
Cancer Drug ◽  
Cancer Cell Growth ◽  
Clock Gene Expression ◽  
Central Pacemaker

Circadian rhythms regulate many physiological and behavioral processes, including sleep, metabolism and cell division, which have a 24-h oscillation pattern. Rhythmicity is generated by a transcriptional–translational feedback loop in individual cells, which are synchronized by the central pacemaker in the brain and external cues. Epidemiological and clinical studies indicate that disruption of these rhythms can increase both tumorigenesis and cancer progression. Environmental changes (shift work, jet lag, exposure to light at night), mutations in circadian regulating genes, and changes to clock gene expression are recognized forms of disruption and are associated with cancer risk and/or cancer progression. Experimental data in animals and cell cultures further supports the role of the cellular circadian clock in coordinating cell division and DNA repair, and disrupted cellular clocks accelerate cancer cell growth. This review will summarize studies linking circadian disruption to cancer biology and explore how such disruptions may be further altered by common characteristics of tumors including hypoxia and acidosis. We will highlight how circadian rhythms might be exploited for cancer drug development, including how delivery of current chemotherapies may be enhanced using chronotherapy. Understanding the role of circadian rhythms in carcinogenesis and tumor progression will enable us to better understand causes of cancer and how to treat them.

Conservative Political Thought in Britain in Response to the French Revolution

1986 ◽  
Vol 29 (3) ◽  
pp. 601-622 ◽  
Author(s):  
Thomas Philip Schofield
Keyword(s):  
Eighteenth Century ◽  
French Revolution ◽  
Social Order ◽  
Glorious Revolution ◽  
True Nature ◽  
The Status ◽  
The Stability ◽  
The Glorious Revolution ◽  
The French Revolution

In attempting to explain the stability of eighteenth-century Britain, and in particular the maintenance of political, social and economic supremacy by the landed aristocracy, scholars have begun to pay attention to the role of ideology and opinion. They see this not merely as providing an explanation of the way things were, but justifying and reinforcing them. The dominant ideological interpretation of society had emerged from the political and constitutional struggles of the seventeenth century, and in particular from the Glorious Revolution of 1688, an interpretation which might be denominated ‘Whig’, and which faced its most serious challenge at the very end of the eighteenth century from the French revolution. Despite the more tangible threat of French arms, the ruling classes in Britain did not underestimate the danger to social order from the arguments advanced by adherents of the rights-of-man doctrine propagated by the revolutionaries. If, in reply to these views, the status quo could be shown not only to be necessary and inevitable, but also right and good, that is to say correspondent with the true nature of man, then the morality of the existing practices and institutions of civil society would be proven. The problem at its most fundamental level was ethical, and it was a problem which conservatives attempted to solve in a variety of ways.

scholarly journals Autophagy and Its Role in Protein Secretion: Implications for Cancer Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Israel Cotzomi-Ortega ◽  
Patricia Aguilar-Alonso ◽  
Julio Reyes-Leyva ◽  
Paola Maycotte
Keyword(s):  
Cancer Therapy ◽  
Cancer Progression ◽  
Protein Secretion ◽  
Survival Function ◽  
Degradation Pathway ◽  
Intercellular Signaling ◽  
Tumor Survival ◽  
Response To Stress ◽  
Secretion Pathways

Autophagy is a protein and organelle degradation pathway important for the maintenance of cytoplasmic homeostasis and for providing nutrients for survival in response to stress conditions. Recently, autophagy has been shown to be important for the secretion of diverse proteins involved in inflammation, intercellular signaling, and cancer progression. The role of autophagy in cancer depends on the stage of tumorigenesis, serving a tumor-suppressor role before transformation and a tumor-survival function once a tumor is established. We review recent evidence demonstrating the complexity of autophagy regulation during cancer, considering the interaction of autophagy with protein secretion pathways. Autophagy manipulation during cancer treatment is likely to affect protein secretion andinter-cellular signaling either to the neighboring cancer cells or to the antitumoral immune response. This will be an important consideration during cancer therapy since several clinical trials are trying to manipulate autophagy in combination with chemotherapy for the treatment of diverse types of cancers.

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.

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