The extracellular matrix modulates the hallmarks of cancer
Reads0
Chats0
TLDR
It is suggested that the success of cancer prevention and therapy programs requires an intimate understanding of the reciprocal feedback between the evolving extracellular matrix, the tumor cells and its cancer‐associated cellular stroma.Abstract:
The extracellular matrix regulates tissue development and homeostasis, and its dysregulation contributes to neoplastic progression. The extracellular matrix serves not only as the scaffold upon which tissues are organized but provides critical biochemical and biomechanical cues that direct cell growth, survival, migration and differentiation and modulate vascular development and immune function. Thus, while genetic modifications in tumor cells undoubtedly initiate and drive malignancy, cancer progresses within a dynamically evolving extracellular matrix that modulates virtually every behavioral facet of the tumor cells and cancer-associated stromal cells. Hanahan and Weinberg defined the hallmarks of cancer to encompass key biological capabilities that are acquired and essential for the development, growth and dissemination of all human cancers. These capabilities include sustained proliferation, evasion of growth suppression, death resistance, replicative immortality, induced angiogenesis, initiation of invasion, dysregulation of cellular energetics, avoidance of immune destruction and chronic inflammation. Here, we argue that biophysical and biochemical cues from the tumor-associated extracellular matrix influence each of these cancer hallmarks and are therefore critical for malignancy. We suggest that the success of cancer prevention and therapy programs requires an intimate understanding of the reciprocal feedback between the evolving extracellular matrix, the tumor cells and its cancer-associated cellular stroma.read more
Citations
More filters
Journal ArticleDOI
Role of Complex Networks for Integrating Medical Images and Radiomic Features of Intracranial Ependymoma Patients in Response to Proton Radiotherapy.
Marco Dominietto,Marco Dominietto,Alessia Pica,Sairos Safai,Antony J. Lomax,Damien C. Weber,Damien C. Weber,Enrico Capobianco +7 more
TL;DR: The challenge of spatially characterizing intratumor heterogeneity is tackled by a network approach that presents two main advantages: Increased detection in the image domain power from high spatial resolution, and Superior accuracy in generating hypotheses underlying clinical decisions.
Journal ArticleDOI
Proteomic Identification of a Gastric Tumor ECM Signature Associated With Cancer Progression
Ana Margarida Moreira,Rui M. Ferreira,Patrícia Carneiro,Joana Figueiredo,Hugo Osório,José Barbosa,John Preto,Perpétua Pinto-do-Ó,Fátima Carneiro,Raquel Seruca +9 more
TL;DR: An extensive characterization of human gastric mucosa is performed, revealing a common ECM signature composed of 142 proteins and indicated that gastric carcinogenesis encompasses ECM remodeling through alterations in the abundance of 24 components, mainly basement membrane proteins.
Journal ArticleDOI
Precise Deposition of Polydopamine on Cancer Cell Membrane as Artificial Receptor for Targeted Drug Delivery.
Hoda Safari Yazd,Yu Yang,Yu Yang,Long Li,Lu Yang,Xiaowei Li,Xiaoshu Pan,Zhuo Chen,Jian-Hui Jiang,Cheng Cui,Weihong Tan,Weihong Tan +11 more
TL;DR: This study uses high K+ and high H2O2 of the tumor microenvironment (TME) to produce polydopamine only on living cancer cell membrane to generate artificial cell surface receptors specific to diseased cells and improve therapeutic efficacy, and decrease the minimum effective dosage.
Journal ArticleDOI
Reduced hyaluronan cross-linking induces breast cancer malignancy in a CAF-dependent manner
TL;DR: In this article, the role of cross-linked hyaluronan cross-linking in breast cancer malignancy was investigated, and it was shown that the deficiency of crosslinked HA induced breast cancer in a CAF-dependent manner, suggesting that recovering HA cross-link may be a potential therapeutic strategy.
Journal ArticleDOI
Biomechanical regulation of breast cancer metastasis and progression.
Adrianne Spencer,Andrew D. Sligar,Daniel Chavarria,Jason Lee,Darshil Choksi,Nikita P. Patil,HooWon Lee,Austin Veith,William J. Riley,Shubh Desai,Ali Abbaspour,Rohan Singeetham,Aaron B. Baker +12 more
TL;DR: In this paper, the role of mechanical forces in altering the chemoresistance, proliferation and metastasis of breast cancer cells was investigated and it was shown that applied mechanical tension can dramatically alter gene expression in breast cancer, leading to decreased proliferation, increased resistance to chemotherapeutic treatment and enhanced adhesion to inflamed endothelial cells and collagen I under fluidic shear stress.
References
More filters
Journal ArticleDOI
Hallmarks of cancer: the next generation.
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
Journal ArticleDOI
The hallmarks of cancer.
TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
Journal ArticleDOI
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
Journal ArticleDOI
Role of YAP/TAZ in mechanotransduction
Sirio Dupont,Leonardo Morsut,Mariaceleste Aragona,Elena Enzo,Stefano Giulitti,Michelangelo Cordenonsi,Francesca Zanconato,Jimmy Le Digabel,Mattia Forcato,Silvio Bicciato,Nicola Elvassore,Stefano Piccolo +11 more
TL;DR: YAP/TAZ are identified as sensors and mediators of mechanical cues instructed by the cellular microenvironment and are functionally required for differentiation of mesenchymal stem cells induced by ECM stiffness and for survival of endothelial cells regulated by cell geometry.
Journal ArticleDOI
Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin Signaling
Kandice R. Levental,Hongmei Yu,Laura Kass,Johnathon N. Lakins,Mikala Egeblad,Janine T. Erler,Sheri F. T. Fong,Katalin Csiszar,Amato J. Giaccia,Wolfgang Weninger,Mitsuo Yamauchi,David L. Gasser,Valerie M. Weaver +12 more
TL;DR: Reduction of lysyl oxidase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and PI3K activity, impeded malignancy, and lowered tumor incidence, and data show how collagenCrosslinking can modulate tissue fibrosis and stiffness to force focal adhesion, growth factor signaling and breast malignancies.