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Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity
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SYSNO ASEP 0555643 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity Tvůrce(i) Kvokačková, Barbora (BFU-R) ORCID
Remsik, J. (US)
Jolly, M. K. (IN)
Souček, Karel (BFU-R) RID, ORCIDCelkový počet autorů 4 Číslo článku 2188 Zdroj.dok. Cancers (Basel). - : MDPI
Roč. 13, č. 9 (2021)Poč.str. 20 s. Forma vydání Online - E Jazyk dok. eng - angličtina Země vyd. CH - Švýcarsko Klíč. slova circulating tumor-cells ; e-cadherin ; stem-cells ; prognostic value ; down-regulation ; metastatic colonization Obor OECD Oncology CEP NV18-08-00245 GA MZd - Ministerstvo zdravotnictví GA20-22984S GA ČR - Grantová agentura ČR Způsob publikování Open access Institucionální podpora BFU-R - RVO:68081707 UT WOS 000649879200001 EID SCOPUS 85104978926 DOI 10.3390/cancers13092188 Anotace 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.
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.Pracoviště Biofyzikální ústav Kontakt Jana Poláková, polakova@ibp.cz, Tel.: 541 517 244 Rok sběru 2022 Elektronická adresa https://www.mdpi.com/2072-6694/13/9/2188
Počet záznamů: 1