2021
Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity
KVOKAČKOVÁ, Barbora; Ján REMŠÍK; Mohit Kumar JOLLY a Karel SOUČEKZákladní údaje
Originální název
Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity
Autoři
KVOKAČKOVÁ, Barbora; Ján REMŠÍK; Mohit Kumar JOLLY a Karel SOUČEK
Vydání
Cancers, Basel, MDPI, 2021, 2072-6694
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30204 Oncology
Stát vydavatele
Švýcarsko
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 6.575
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/21:00121663
Organizační jednotka
Přírodovědecká fakulta
UT WoS
EID Scopus
Klíčová slova anglicky
triple-negative breast cancer; plasticity; epithelial– mesenchymal transition; mesenchymal– epithelial transition; metastasis
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 28. 5. 2021 11:48, Mgr. Marie Novosadová Šípková, DiS.
Anotace
V originále
Triple-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.
Návaznosti
| EF16_025/0007381, projekt VaV |
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