MITF depletion elevates expression levels of ERBB3 receptor and its cognate ligand NRG1-beta in melanoma

被引：11

作者：

Alver, Tine N. ^{[1
]}

Lavelle, Timothy J. ^{[1
]}

Longva, Ane S. ^{[1
]}

Oy, Geir F. ^{[1
]}

Hovig, Eivind ^{[1
,2
,3
]}

Boe, Sigurd L. ^{[1
]}

机构：

[1] Oslo Univ Hosp, Inst Canc Res, Dept Tumor Biol, Oslo, Norway

[2] Oslo Univ Hosp, Inst Canc Genet & Informat, Norwegian Radium Hosp, Oslo, Norway

[3] Univ Oslo, Dept Informat, Oslo, Norway

来源：

ONCOTARGET | 2016年 / 7卷 / 34期

关键词：

MITF; ERBB3; NRG1-beta; PI3K signaling; melanoma; UP-REGULATION; FEEDBACK INHIBITION; RAF INHIBITORS; RESISTANCE; CELLS; TRANSCRIPTION; KINASE; SOX10; ANTIBODIES; SURVIVAL;

D O I：

10.18632/oncotarget.10422

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway is frequently hyper-activated upon vemurafenib treatment of melanoma. We have here investigated the relationship between SRY-box 10 (SOX10), forkhead box 3 (FOXD3) and microphthalmia-associated transcription factor (MITF) in the regulation of the receptor tyrosine-protein kinase ERBB3, and its cognate ligand neuregulin 1-beta (NRG1-beta). We found that both NRG1-beta and ERBB3 mRNA levels were elevated as a consequence of MITF depletion, induced by either vemurafenib or MITF small interfering RNA (siRNA) treatment. Elevation of ERBB3 receptor expression after MITF depletion caused increased activation of the PI3K pathway in the presence of NRG1-beta ligand. Together, our results suggest that MITF may play a role in the development of acquired drug resistance through hyper-activation of the PI3K pathway.

引用

页码：55128 / 55140

页数：13

共 35 条

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