Publisher Correction: The low affinity neurotrophin receptor CD271 regulates phenotype switching in melanoma

Abstract

The originally published version of this Article was updated shortly after publication to add the words 'The' and 'affinity' to the title, following their inadvertent removal during the production process. This has now been corrected in both the PDF and HTML versions of the Article.

Decoding the Role of CD271 in Melanoma

“…In addition, the decrease of CD271 significantly reduced the capability of tumor formation in vivo and cell migration in vitro [ 40 , 44 , 50 ]. On the other hand, the overexpression of CD271 increased levels of SOX2 and RHOJ and the propensity of migration and metastasis of A375 cells [ 43 , 53 ]; however, the underlying mechanisms are poorly understood. These experiments strongly suggest a more comprehensive role of CD271, serving as determinant of melanoma cell properties independent from the presence of a BRAF V600E -mutation.…”

“…Recently, the expression of CD271 was recognized as a regulator of phenotype switching, a process that enables the rapid and reversible conversion of non-stem-like into stem-like or proliferative into invasive states. The latter was associated with the AXL high /MITF low program [ 53 , 54 , 55 , 56 , 57 , 58 ]. In addition, Hoek et al specified the proliferative/low-migratory phenotype by (1) the levels of MITF-targets (TYR, DCT, PMEL, MLANA), (2) NC-related genes (SOX10, TFAP1A, EDNRB), and (3) the sensitivity toward the growth-inhibitory effect of TGF-β and the proportion of Ki67-positive cells [ 80 , 81 ].…”

“…In addition, Hoek et al specified the proliferative/low-migratory phenotype by (1) the levels of MITF-targets (TYR, DCT, PMEL, MLANA), (2) NC-related genes (SOX10, TFAP1A, EDNRB), and (3) the sensitivity toward the growth-inhibitory effect of TGF-β and the proportion of Ki67-positive cells [ 80 , 81 ]. Contrary, the migratory/low-proliferative phenotype was specified by EMT-inducers ZEB1, TWIST1, and c-JUN as well as CD271 and AXL [ 53 , 82 ]. The conditional overexpression of CD271 in melanoma cell lines impaired the proliferation in vitro and in vivo but enhanced metastasis formation at distant organs.…”

The role of tumor stem cells in the development of drug resistance of melanoma

“…G. Restivo и соавт. в исследовании показали, что CD271 является ключевым эффектором в переключении фенотипа клеток меланомы [39]. Согласно модели «переключения фенотипов» агрессивный характер клеток меланомы обусловлен их внутренним потенциалом для динамического перехода от высокопролиферативного / низкоинвазивного к низкому пролиферативному / высокоинвазивному состоянию [28,40,41].…”

“…Возобновление пролиферации ОСК на удаленном участке возможно после уменьшения экспрессии CD271. Механически расщепленный внутриклеточный домен CD271 контролирует пролиферацию, тогда как взаимодействие CD271 с рецептором нейротрофина Trk-A модулирует клеточную адгезию и инвазивность [39].…”