J 2021

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

KVOKAČKOVÁ, Barbora; Ján REMŠÍK; Mohit Kumar JOLLY a Karel SOUČEK

Základní 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

EID Scopus

Klíčová slova anglicky

triple-negative breast cancer; plasticity; epithelial– mesenchymal transition; mesenchymal– epithelial transition; metastasis

Štítky

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
Název: Preklinická progrese nových organických sloučenin s cílenou biologickou aktivitou