CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling DOI
Shan Wang, Emelie Englund,

Pontus Kjellman

et al.

Nature Cell Biology, Journal Year: 2021, Volume and Issue: 23(7), P. 758 - 770

Published: July 1, 2021

Language: Английский

The matrix in cancer DOI
Thomas R. Cox

Nature reviews. Cancer, Journal Year: 2021, Volume and Issue: 21(4), P. 217 - 238

Published: Feb. 15, 2021

Language: Английский

Citations

678

Long noncoding RNAs in cancer metastasis DOI
Siyuan Liu, Ha X. Dang, Daniel A. Lim

et al.

Nature reviews. Cancer, Journal Year: 2021, Volume and Issue: 21(7), P. 446 - 460

Published: May 5, 2021

Language: Английский

Citations

501

Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments DOI Creative Commons
Zhennan Yuan, Yingpu Li, Sifan Zhang

et al.

Molecular Cancer, Journal Year: 2023, Volume and Issue: 22(1)

Published: March 11, 2023

The malignant tumor is a multi-etiological, systemic and complex disease characterized by uncontrolled cell proliferation distant metastasis. Anticancer treatments including adjuvant therapies targeted are effective in eliminating cancer cells but limited number of patients. Increasing evidence suggests that the extracellular matrix (ECM) plays an important role development through changes macromolecule components, degradation enzymes stiffness. These variations under control cellular components tissue via aberrant activation signaling pathways, interaction ECM to multiple surface receptors, mechanical impact. Additionally, shaped regulates immune which results suppressive microenvironment hinders efficacy immunotherapies. Thus, acts as barrier protect from supports progression. Nevertheless, profound regulatory network remodeling hampers design individualized antitumor treatment. Here, we elaborate on composition ECM, discuss specific mechanisms remodeling. Precisely, highlight impact development, proliferation, anoikis, metastasis, angiogenesis, lymphangiogenesis, escape. Finally, emphasize "normalization" potential strategy for anti-malignant

Language: Английский

Citations

368

Targeting FAK in anticancer combination therapies DOI
John C. Dawson, Alan Serrels, Dwayne G. Stupack

et al.

Nature reviews. Cancer, Journal Year: 2021, Volume and Issue: 21(5), P. 313 - 324

Published: March 17, 2021

Language: Английский

Citations

263

Drug resistance and Cancer stem cells DOI Creative Commons
Yuan Li, Zhenning Wang, Jaffer A. Ajani

et al.

Cell Communication and Signaling, Journal Year: 2021, Volume and Issue: 19(1)

Published: Feb. 15, 2021

Abstract Therapy resistance is a major problem when treating cancer patients as cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones contribute poor prognosis. can be both intrinsic and/or acquired. These are multifactorial events, some related factors including adaptations in stem (CSCs), epithelial-mesenchymal transition (EMT), deregulation key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, activation DNA damage response among others. Among these factors, CSCs represent source therapy resistance. subset tumor capable self-renewal multilineage progenitor expansion known intrinsically resistant anticancer treatments. Multiple pre-exist, adopt expand easily changes microenvironment (TME) radio- chemotherapy. A combination extrinsic contributes CSC-mediated In this review, we will focus on well suggest strategies eliminate and, therefore, overcome

Language: Английский

Citations

231

Towards targeting of shared mechanisms of cancer metastasis and therapy resistance DOI
Felix Weiß, Douglas A. Lauffenburger, Peter Friedl

et al.

Nature reviews. Cancer, Journal Year: 2022, Volume and Issue: 22(3), P. 157 - 173

Published: Jan. 10, 2022

Language: Английский

Citations

193

Breast Cancer Stem Cells as Drivers of Tumor Chemoresistance, Dormancy and Relapse: New Challenges and Therapeutic Opportunities DOI Open Access
Maria Laura De Angelis, Federica Francescangeli, Ann Zeuner

et al.

Cancers, Journal Year: 2019, Volume and Issue: 11(10), P. 1569 - 1569

Published: Oct. 15, 2019

Breast cancer is the most frequent among women worldwide. Therapeutic strategies to prevent or treat metastatic disease are still inadequate although great progress has been made in treating early-stage breast cancer. Cancer stem-like cells (CSCs) that endowed with high plasticity and self-renewal properties have shown play a key role development, progression, metastasis. A subpopulation of CSCs combines tumor-initiating capacity dormant/quiescent/slow cycling status present throughout clinical history patients. Dormant/quiescent/slow component tumor heterogeneity they responsible for chemoresistance, migration, dormancy, defined as ability survive target organs generate metastasis up two decades after diagnosis. Understanding used by resist conventional targeted therapies, interact their niche, escape immune surveillance, finally awaken from dormancy importance This review summarizes current understanding mechanisms involved dissemination, cancer, particular focus on dormant cells. Finally, we discuss how advancements detection, molecular understanding, targeting will likely open new therapeutic avenues treatment.

Language: Английский

Citations

149

YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches DOI
Stefano Piccolo, Tito Panciera, Paolo Contessotto

et al.

Nature Cancer, Journal Year: 2022, Volume and Issue: unknown

Published: Dec. 23, 2022

Language: Английский

Citations

142

The epithelial-mesenchymal transition and the cytoskeleton in bioengineered systems DOI Creative Commons
Susan E. Leggett,

Alex M. Hruska,

Ming Guo

et al.

Cell Communication and Signaling, Journal Year: 2021, Volume and Issue: 19(1)

Published: March 10, 2021

Abstract The epithelial-mesenchymal transition (EMT) is intrinsically linked to alterations of the intracellular cytoskeleton and extracellular matrix. After EMT, cells acquire an elongated morphology with front/back polarity, which can be attributed actin-driven protrusion formation as well gain vimentin expression. Consequently, deform remodel surrounding matrix in order facilitate local invasion. In this review, we highlight recent bioengineering approaches elucidate EMT functional changes cytoskeleton. First, review transitions between multicellular clusters dispersed individuals on planar surfaces, often exhibit coordinated behaviors driven by leader EMT. Second, consider role vimentin, probed at subcellular length scales within confined spaces. Third, discuss topographical patterning via a contact guidance like mechanism. Finally, address how disorganize disseminate 3D These new technologies enable controlled physical microenvironments higher-resolution spatiotemporal measurements single cell level. closing, future directions for field outstanding questions regarding human cancer progression.

Language: Английский

Citations

118

Biological role of matrix stiffness in tumor growth and treatment DOI Creative Commons
Boer Deng, Ziyi Zhao, Wei­min Kong

et al.

Journal of Translational Medicine, Journal Year: 2022, Volume and Issue: 20(1)

Published: Nov. 22, 2022

Abstract In recent years, the biological role of changes in physical factors carcinogenesis and progression has attracted increasing attention. Matrix stiffness, also known as ECM stress, is a critical factor tumor microenvironment remains alternating during result remodeling through activation cancer-associated fibroblasts extracellular collagen accumulation, crosslinking fibrosis. Different content density endows matrix with varying stiffness. Physical signals induced by stiffness are transmitted to cells primarily integrins receptor family trigger series mechanotransduction that cell morphology, proliferative capacity, invasive ability. Importantly, accumulating evidence revealed tissues greatly control sensitivity response chemotherapy, radiotherapy, immunotherapy integrin signaling, YAP related signaling pathways. Here, present review analyzes current research advances on behavior view contributing growth treatment, hope improving understanding tumors.

Language: Английский

Citations

115