Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F21%3A00555643" target="_blank" >RIV/68081707:_____/21:00555643 - isvavai.cz</a>

Alternative codes found

RIV/00159816:_____/21:00075117 RIV/00216224:14310/21:00121663

Result on the web

<a href="https://www.mdpi.com/2072-6694/13/9/2188" target="_blank" >https://www.mdpi.com/2072-6694/13/9/2188</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/cancers13092188" target="_blank" >10.3390/cancers13092188</a>

Result language

angličtina

Original language name

Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity

Original language description

Epithelial-mesenchymal transition (EMT) and its reverse process mesenchymal-epithelial transition (MET) are considered critical events in the cancer progression. These programs are tightly connected with the development of metastasis-the lethal stage of the disease. Both EMT and MET shape the biology of unusually aggressive and heterogeneous triple-negative breast cancer (TNBC). In this review, we summarize the current knowledge of EMT/MET plasticity in the context of TNBC, with a special focus on drivers and mechanisms behind these processes.nnTriple-negative breast cancer (TNBC) is a subtype of breast carcinoma known for its unusually aggressive behavior and poor clinical outcome. Besides the lack of molecular targets for therapy and profound intratumoral heterogeneity, the relatively quick overt metastatic spread remains a major obstacle in effective clinical management. The metastatic colonization of distant sites by primary tumor cells is affected by the microenvironment, epigenetic state of particular subclones, and numerous other factors. One of the most prominent processes contributing to the intratumoral heterogeneity is an epithelial-mesenchymal transition (EMT), an evolutionarily conserved developmental program frequently hijacked by tumor cells, strengthening their motile and invasive features. In response to various intrinsic and extrinsic stimuli, malignant cells can revert the EMT state through the mesenchymal-epithelial transition (MET), a process that is believed to be critical for the establishment of macrometastasis at secondary sites. Notably, cancer cells rarely undergo complete EMT and rather exist in a continuum of E/M intermediate states, preserving high levels of plasticity, as demonstrated in primary tumors and, ultimately, in circulating tumor cells, representing a simplified element of the metastatic cascade. In this review, we focus on cellular drivers underlying EMT/MET phenotypic plasticity and its detrimental consequences in the context of TNBC cancer.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30204 - Oncology

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2021

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Cancers (Basel)

ISSN

2072-6694

e-ISSN

2072-6694

Volume of the periodical

13

Issue of the periodical within the volume

9

Country of publishing house

CH - SWITZERLAND

Number of pages

20

Pages from-to

2188

UT code for WoS article

000649879200001

EID of the result in the Scopus database

2-s2.0-85104978926