scholarly journals An NFκB-dependent mechanism of tumor cell plasticity and lateral transmission of aggressive features

Oncotarget ◽  
2018 ◽  
Vol 9 (42) ◽  
pp. 26679-26700 ◽  
Author(s):  
Nancy Adriana Espinoza-Sánchez ◽  
Jennifer Enciso ◽  
Rosana Pelayo ◽  
Ezequiel M. Fuentes-Pananá
Keyword(s):  
Tumor Cell ◽  
Cell Plasticity ◽  
Tumor Cell Plasticity ◽  
Lateral Transmission ◽  
Dependent Mechanism

scholarly journals The Intimate Relationship among EMT, MET and TME: A T(ransdifferentiation) E(nhancing) M(ix) to Be Exploited for Therapeutic Purposes

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3674 ◽  
Author(s):  
Ralf Hass ◽  
Juliane von der Ohe ◽  
Hendrik Ungefroren
Keyword(s):  
Stem Cell ◽  
Phenotypic Plasticity ◽  
Tumor Cell ◽  
Epithelial Mesenchymal Transition ◽  
Resistance Mechanisms ◽  
Current Evidence ◽  
Cell Plasticity ◽  
New Paradigm ◽  
Mesenchymal Transition ◽  
Tumor Cell Plasticity

Intratumoral heterogeneity is considered the major cause of drug unresponsiveness in cancer and accumulating evidence implicates non-mutational resistance mechanisms rather than genetic mutations in its development. These non-mutational processes are largely driven by phenotypic plasticity, which is defined as the ability of a cell to reprogram and change its identity (phenotype switching). Tumor cell plasticity is characterized by the reactivation of developmental programs that are closely correlated with the acquisition of cancer stem cell properties and an enhanced potential for retrodifferentiation or transdifferentiation. A well-studied mechanism of phenotypic plasticity is the epithelial-mesenchymal transition (EMT). Current evidence suggests a complex interplay between EMT, genetic and epigenetic alterations, and clues from the tumor microenvironment in cell reprogramming. A deeper understanding of the connections between stem cell, epithelial–mesenchymal, and tumor-associated reprogramming events is crucial to develop novel therapies that mitigate cell plasticity and minimize the evolution of tumor heterogeneity, and hence drug resistance. Alternatively, vulnerabilities exposed by tumor cells when residing in a plastic or stem-like state may be exploited therapeutically, i.e., by converting them into less aggressive or even postmitotic cells. Tumor cell plasticity thus presents a new paradigm for understanding a cancer’s resistance to therapy and deciphering its underlying mechanisms.

Functional role of matrix metalloproteinases in ovarian tumor cell plasticity

2004 ◽  
Vol 190 (4) ◽  
pp. 899-909 ◽  
Author(s):  
Anil K. Sood ◽  
Mavis S. Fletcher ◽  
Jeremy E. Coffin ◽  
Maria Yang ◽  
Elisabeth A. Seftor ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Tumor Cell ◽  
Ovarian Tumor ◽  
Functional Role ◽  
Cell Plasticity ◽  
Ovarian Tumor Cell ◽  
Tumor Cell Plasticity

Prostatic tumor cell plasticity involves cooperative interactions of distinct phenotypic subpopulations: Role in vasculogenic mimicry

The Prostate ◽  
2002 ◽  
Vol 50 (3) ◽  
pp. 189-201 ◽  
Author(s):  
Navesh Sharma ◽  
Richard E.B. Seftor ◽  
Elisabeth A. Seftor ◽  
Lynn M. Gruman ◽  
Paul M. Heidger ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Vasculogenic Mimicry ◽  
Cell Plasticity ◽  
Cooperative Interactions ◽  
Tumor Cell Plasticity ◽  
Prostatic Tumor
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