The Influence of Polymeric Fiber Stiffness and Alignment on Cytoplasmic Bleb Dynamics and Migration of Glioblastoma Multiforme Cells

2012 ◽  
Author(s):  
Puja Sharma ◽  
Kevin Sheets ◽  
Amrinder S. Nain
Keyword(s):  
Immune Response ◽  
Wound Healing ◽  
Cell Migration ◽  
Glioblastoma Multiforme ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Hallmarks Of Cancer ◽  
Multistep Process ◽  
And Migration ◽  
Polymeric Fiber

Cell migration is a tightly regulated phenomenon necessary for regular physiologic processes such as wound healing, immune response, embryonic development, growth, and regeneration [1–3]. Consequences of abnormal migratory behaviors include autoimmune diseases and metastasis during cancer progression [4, 5]. Described as one of the hallmarks of cancer, metastasis is a complex multistep process, and is responsible for 90% of cancer deaths in humans. A better understanding of the process of metastasis is of paramount importance in developing efficient cancer treatment therapies and drugs [6].

Adipose tissue, obesity and adipokines: role in cancer promotion

2015 ◽  
Vol 21 (1) ◽  
Author(s):  
Andrea Booth ◽  
Aaron Magnuson ◽  
Josephine Fouts ◽  
Michelle Foster
Keyword(s):  
Adipose Tissue ◽  
Cancer Risk ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Epidemiological Studies ◽  
Normal Weight ◽  
Cell Progression ◽  
High Cancer Risk ◽  
Apoptosis Pathways ◽  
And Migration

AbstractAdipose tissue is a complex organ with endocrine, metabolic and immune regulatory roles. Adipose depots have been characterized to release several adipocytokines that work locally in an autocrine and paracrine fashion or peripherally in an endocrine fashion. Adipocyte hypertrophy and excessive adipose tissue accumulation, as occurs during obesity, dysregulates the microenvironment within adipose depots and systemically alters peripheral tissue metabolism. The term “adiposopathy” is used to describe this promotion of pathogenic adipocytes and associated adipose – elated disorders. Numerous epidemiological studies confirm an association between obesity and various cancer forms. Proposed mechanisms that link obesity/adiposity to high cancer risk and mortality include, but are not limited to, obesity-related insulin resistance, hyperinsulinemia, sustained hyperglycemia, glucose intolerance, oxidative stress, inflammation and/or adipocktokine production. Several epidemiological studies have demonstrated a relationship between specific circulating adipocytokines and cancer risk. The aim of this review is to define the function, in normal weight and obesity states, of well-characterized and novel adipokines including leptin, adiponectin, apelin, visfatin, resistin, chemerin, omentin, nesfatin and vaspin and summarize the data that relates their dysfunction, whether associated or direct effects, to specific cancer outcomes. Overall research suggests most adipokines promote cancer cell progression via enhancement of cell proliferation and migration, inflammation and anti-apoptosis pathways, which subsequently can prompt cancer metastasis. Further research and longitudinal studies are needed to define the specific independent and additive roles of adipokines in cancer progression and reoccurrence.

scholarly journals Fingering instability in spreading epithelial monolayers: roles of cell polarisation, substrate friction and contractile stresses

Soft Matter ◽  
2021 ◽  
Author(s):  
Carolina Trenado ◽  
Luis L. Bonilla ◽  
Alejandro Martínez-Calvo
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cancer Progression ◽  
Coherent Structures ◽  
Crucial Role ◽  
Collective Cell Migration ◽  
Developmental Processes ◽  
Epithelial Monolayers ◽  
Fingering Instability

Collective cell migration plays a crucial role in many developmental processes that underlie morphogenesis, wound healing, or cancer progression. In such coordinated behaviours, cells are organised in coherent structures and...

scholarly journals Jamming in Embryogenesis and Cancer Progression

2021 ◽  
Vol 9 ◽  
Author(s):  
Eliane Blauth ◽  
Hans Kubitschke ◽  
Pablo Gottheil ◽  
Steffen Grosser ◽  
Josef A. Käs
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Resting State ◽  
Biological Processes ◽  
Number Density ◽  
Biological Factors ◽  
Jamming Transition

The ability of tissues and cells to move and rearrange is central to a broad range of diverse biological processes such as tissue remodeling and rearrangement in embryogenesis, cell migration in wound healing, or cancer progression. These processes are linked to a solid-like to fluid-like transition, also known as unjamming transition, a not rigorously defined framework that describes switching between a stable, resting state and an active, moving state. Various mechanisms, that is, proliferation and motility, are critical drivers for the (un)jamming transition on the cellular scale. However, beyond the scope of these fundamental mechanisms of cells, a unifying understanding remains to be established. During embryogenesis, the proliferation rate of cells is high, and the number density is continuously increasing, which indicates number-density-driven jamming. In contrast, cells have to unjam in tissues that are already densely packed during tumor progression, pointing toward a shape-driven unjamming transition. Here, we review recent investigations of jamming transitions during embryogenesis and cancer progression and pursue the question of how they might be interlinked. We discuss the role of density and shape during the jamming transition and the different biological factors driving it.

scholarly journals SPTBN2 regulated by miR-424-5p promotes endometrial cancer progression via CLDN4/PI3K/AKT axis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Pengling Wang ◽  
Ting Liu ◽  
Zhendan Zhao ◽  
Zhiling Wang ◽  
Shujie Liu ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Migration ◽  
Cancer Progression ◽  
Poor Prognosis ◽  
Cancer Metastasis ◽  
Prognostic Biomarker ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Endometrioid Endometrial Cancer ◽  
Metastasis Therapy

AbstractEndometrioid Endometrial Cancer (EEC) is the main subtype of endometrial cancer. In our study, we demonstrated that SPTBN2 was significantly overexpressed in EEC tissues. Upregulated SPTBN2 expression was positively associated with poor prognosis. In addition, we testified that SPTBN2 knockdown significantly inhibited the proliferation, migration, and invasion of EEC cells. Moreover, we found SPTBN2 could interact with CLDN4 to promote endometrial cancer metastasis via PI3K/AKT pathway. Then we further demonstrated that CLDN4 is upregulated in EEC and promotes EEC metastasis. CLDN4 overexpression could partially reversed the decrease in cell migration and invasion caused by SPTBN2 downregulation. In addition, we confirmed that SPTBN2 was a target of miR-424-5p, which plays a tumor suppressor in endometrial cancer. Rescue experiments showed that inhibition of SPTBN2 could partially reverse the effect of miR-424-5p in EEC. In conclusion, we demonstrated that by acting as a significant target of miR-424-5p, SPTBN2 could interact with CLDN4 to promote endometrial cancer metastasis via PI3K/AKT pathway in EEC. Our study revealed the prognostic and metastatic effects of SPTBN2 in EEC, suggesting that SPTBN2 could serve as a prognostic biomarker and a target for metastasis therapy.

scholarly journals Epithelial-to-Mesenchymal Transition in the Light of Plasticity and Hybrid E/M States

2021 ◽  
Vol 10 (11) ◽  
pp. 2403
Author(s):  
Laura Bornes ◽  
Guillaume Belthier ◽  
Jacco van Rheenen
Keyword(s):  
Wound Healing ◽  
Cell Adhesion ◽  
Basement Membrane ◽  
Cell Polarity ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Therapy Resistance ◽  
Mesenchymal Transition

Epithelial-to-mesenchymal transition (EMT) is a cellular program which leads to cells losing epithelial features, including cell polarity, cell–cell adhesion and attachment to the basement membrane, while gaining mesenchymal characteristics, such as invasive properties and stemness. This program is involved in embryogenesis, wound healing and cancer progression. Over the years, the role of EMT in cancer progression has been heavily debated, and the requirement of this process in metastasis even has been disputed. In this review, we discuss previous discrepancies in the light of recent findings on EMT, plasticity and hybrid E/M states. Moreover, we highlight various tumor microenvironmental cues and cell intrinsic signaling pathways that induce and sustain EMT programs, plasticity and hybrid E/M states. Lastly, we discuss how recent findings on plasticity, especially on those that enable cells to switch between hybrid E/M states, have changed our understanding on the role of EMT in cancer metastasis, stemness and therapy resistance.

scholarly journals DOCK1 Regulates Growth and Motility through the RRP1B-Claudin-1 Pathway in Claudin-Low Breast Cancer Cells

Cancers ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1762 ◽  
Author(s):  
Chiang ◽  
Chang ◽  
Chen ◽  
Chang
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Dna Methyltransferase ◽  
Cancer Metastasis ◽  
Metastatic Potential ◽  
Significant Inhibition ◽  
And Migration

Dedicator of cytokinesis 1 (DOCK1) is a critical regulator of cancer metastasis. Claudins are transmembrane proteins that play a role in epithelial barrier integrity. Due to a loss or low expression of claudins (CLDN), the claudin-low type of triple-negative breast cancer (TNBC) is characterized by a mesenchymal-like phenotype with strong metastatic potential. In order to elucidate the mechanism of DOCK1 in cancer metastasis, we first analyzed the transcriptomic changes using a clinical database of human TNBC and found that the increase in DOCK1 expression was highly correlated with the poor survival rate of TNBC patients. Interference with DOCK1 expression by shRNA resulted in re-expression of claudin-1 in conjunction with significant inhibition of cell viability and motility of claudin-low breast cancer cells. Accordingly, overexpression of claudin-1 suppressed cell viability and migration. Genetic knockdown and pharmacological blockade of Rac1/Rac2 up-regulated claudin-1. DOCK1 knockdown also caused a decrease in DNA methyltransferase (DNMT) expression and an increase in claudin-1 transcript and promoter activity. Furthermore, RRP1B mediated DOCK1 depletion, which up-regulated claudin-1 expression, cell viability, and motility in claudin-low breast cancer cells. This study demonstrated that DOCK1 mediates growth and motility through down-regulated claudin-1 expression via the RRP1BDNMTclaudin-1 pathway and that claudin-1 serves as an important effector in DOCK1-mediated cancer progression and metastasis in claudin-low breast cancer cells.

scholarly journals STIM and ORAI proteins: crucial roles in hallmarks of cancer

2016 ◽  
Vol 310 (7) ◽  
pp. C509-C519 ◽  
Author(s):  
A. Fiorio Pla ◽  
K. Kondratska ◽  
N. Prevarskaya
Keyword(s):  
Cancer Progression ◽  
Cancer Therapeutics ◽  
Cellular Functions ◽  
Hallmarks Of Cancer ◽  
Cellular Processes ◽  
Store Depletion ◽  
Multistep Process ◽  
Intracellular Ca ◽  
Critical Components

Intracellular Ca2+ signals play a central role in several cellular processes; therefore it is not surprising that altered Ca2+ homeostasis regulatory mechanisms lead to a variety of severe pathologies, including cancer. Stromal interaction molecules (STIM) and ORAI proteins have been identified as critical components of Ca2+ entry in both store-dependent (SOCE mechanism) and independent by intracellular store depletion and have been implicated in several cellular functions. In recent years, both STIMs and ORAIs have emerged as possible molecular targets for cancer therapeutics. In this review we focus on the role of STIM and ORAI proteins in cancer progression. In particular we analyze their role in the different hallmarks of cancer, which represent the organizing principle that describes the complex multistep process of neoplastic diseases.

Influence of electrotaxis on cell behaviour

2014 ◽  
Vol 6 (9) ◽  
pp. 817-830 ◽  
Author(s):  
Barbara Cortese ◽  
Ilaria Elena Palamà ◽  
Stefania D'Amone ◽  
Giuseppe Gigli
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cancer Metastasis ◽  
Cell Behaviour ◽  
Physiological Processes ◽  
Neuron Guidance

Understanding the mechanism of cell migration and interaction with the microenvironment is not only of critical significance to the function and biology of cells, but also has extreme relevance and impact on physiological processes and diseases such as morphogenesis, wound healing, neuron guidance, and cancer metastasis.

scholarly journals Tracking of Endothelial Cell Migration and Stiffness Measurements Reveal the Role of Cytoskeletal Dynamics

2022 ◽  
Vol 23 (1) ◽  
pp. 568
Author(s):  
Dominick J. Romano ◽  
Jesus M. Gomez-Salinero ◽  
Zoran Šunić ◽  
Antonio Checco ◽  
Sina Y. Rabbany
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Time Lapse ◽  
Random Force ◽  
Endothelial Cell Migration ◽  
Collective Migration ◽  
Force Microscopy ◽  
Cytoskeletal Dynamics ◽  
Directional Change ◽  
Multistep Process

Cell migration is a complex, tightly regulated multistep process in which cytoskeletal reorganization and focal adhesion redistribution play a central role. Core to both individual and collective migration is the persistent random walk, which is characterized by random force generation and resistance to directional change. We first discuss a model that describes the stochastic movement of ECs and characterizes EC persistence in wound healing. To that end, we pharmacologically disrupted cytoskeletal dynamics, cytochalasin D for actin and nocodazole for tubulin, to understand its contributions to cell morphology, stiffness, and motility. As such, the use of Atomic Force Microscopy (AFM) enabled us to probe the topography and stiffness of ECs, while time lapse microscopy provided observations in wound healing models. Our results suggest that actin and tubulin dynamics contribute to EC shape, compressive moduli, and directional organization in collective migration. Insights from the model and time lapse experiment suggest that EC speed and persistence are directionally organized in wound healing. Pharmacological disruptions suggest that actin and tubulin dynamics play a role in collective migration. Current insights from both the model and experiment represent an important step in understanding the biomechanics of EC migration as a therapeutic target.

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