Secretome from senescent melanoma engages the STAT3 pathway to favor reprogramming of naive melanoma towards a tumor-initiating cell phenotype.
Secretome from senescent melanoma engages the STAT3 pathway to favor reprogramming of naive melanoma towards a tumor-initiating cell phenotype.
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DOI：
10.18632/oncotarget.1143
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发表时间：
2013-12
期刊：
影响因子：
--
通讯作者：
Ballotti R
中科院分区：
文献类型：
--
作者：
Ohanna M;Cheli Y;Bonet C;Bonazzi VF;Allegra M;Giuliano S;Bille K;Bahadoran P;Giacchero D;Lacour JP;Boyle GM;Hayward NF;Bertolotto C;Ballotti R
在这里，我们发现衰老黑色素瘤细胞的分泌组驱动基底黑色素瘤细胞向间充质表型发展，其干细胞的特征由原型基因FN 1、SNAIL、OCT 4和NANOG的水平增加所说明。这种分子重编程导致具有黑色素瘤起始细胞特征的低MITF和生长缓慢的细胞群增加。衰老黑色素瘤细胞的分泌组诱导一组52个基因，参与细胞运动和细胞/细胞相互作用，其中AXL和ALDH 1A 3与黑色素瘤的发展有关。我们发现衰老黑色素瘤细胞的分泌组激活STAT 3通路，并且STAT 3抑制防止分泌组效应，包括致瘤特性的获得。总的来说，这些发现提供了关于在化疗治疗后进入衰老的黑色素瘤细胞的分泌组如何通过STAT 3激活诱导可能有利于化疗耐药性和复发的黑色素瘤起始细胞表型来增加幼稚黑色素瘤细胞的致瘤性的见解。
Here, we showed that the secretome of senescent melanoma cells drives basal melanoma cells towards a mesenchymal phenotype, with characteristic of stems illustrated by increased level of the prototype genes FN1, SNAIL, OCT4 and NANOG. This molecular reprogramming leads to an increase in the low-MITF and slow-growing cell population endowed with melanoma-initiating cell features. The secretome of senescent melanoma cells induces a panel of 52 genes, involved in cell movement and cell/cell interaction, among which AXL and ALDH1A3 have been implicated in melanoma development. We found that the secretome of senescent melanoma cells activates the STAT3 pathway and STAT3 inhibition prevents secretome effects, including the acquisition of tumorigenic properties. Collectively, the findings provide insights into how the secretome of melanoma cells entering senescence upon chemotherapy treatments increases the tumorigenicity of naïve melanoma cells by inducing, through STAT3 activation, a melanoma-initiating cell phenotype that could favor chemotherapy resistance and relapse.
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影响因子：
64.8
作者：
Bertolotto, Corine;Lesueur, Fabienne;Bressac-de Paillerets, Brigitte
通讯作者：
Bressac-de Paillerets, Brigitte
DOI：
10.1146/annurev-pathol-121808-102144
发表时间：
2010
期刊：
Annual review of pathology
影响因子：
--
作者：
Coppé JP;Desprez PY;Krtolica A;Campisi J
通讯作者：
Campisi J
影响因子：
11.5
作者：
Harbst, Katja;Staaf, Johan;Jonsson, Goran
通讯作者：
Jonsson, Goran
影响因子：
10.5
作者：
Ohanna, Mickael;Giuliano, Sandy;Bertolotto, Corine
通讯作者：
Bertolotto, Corine
影响因子：
64.5
作者：
Kuilman, Thomas;Michaloglou, Chrysiis;Peeper, Daniel S.
通讯作者：
Peeper, Daniel S.