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Relief of feedback inhibition of HER3 transcription by RAF and MEK inhibitors attenuates their antitumor effects in BRAF mutant thyroid carcinomas.

ABSTRACT: Analysis of transcriptome kinetics of SW1736 thyroid cancer cell line vs SK-MEL-28 melanoma cell line at various times after addition of 2 µM vemurafenib. The hypothesis tested was that SW1736 cells (vemurafenib-refractory) differentially express genes compared to SK-MEL-28 cells (vemurafenib sensitive) that confer resistance to the RAF inhibitor.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37441 | GEO | 2013/02/01

SECONDARY ACCESSION(S): PRJNA159927

REPOSITORIES: GEO

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Relief of feedback inhibition of HER3 transcription by RAF and MEK inhibitors attenuates their antitumor effects in BRAF mutant thyroid carcinomas.

Project description:Analysis of transcriptome kinetics of SW1736 thyroid cancer cell line vs SK-MEL-28 melanoma cell line at various times after addition of 2 µM vemurafenib. The hypothesis tested was that SW1736 cells (vemurafenib-refractory) differentially express genes compared to SK-MEL-28 cells (vemurafenib sensitive) that confer resistance to the RAF inhibitor. Total RNA was obtained from lysates of SW1726 and SK-MEL-28 cells treated with 2 µM vemurafenib for 0, 1, 6 and 48 h. Experiment was made by triplicate.

2013-02-01 | E-GEOD-37441 | biostudies-arrayexpress

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Relief of feedback inhibition of HER3 transcription by RAF and MEK inhibitors attenuates their antitumor effects in BRAF-mutant thyroid carcinomas.

Project description:The RAF inhibitor vemurafenib (PLX4032) increases survival in patients with BRAF-mutant metastatic melanoma, but has limited efficacy in patients with colorectal cancers. Thyroid cancer cells are also comparatively refractory to RAF inhibitors. In contrast to melanomas, inhibition of mitogen-activated protein kinase (MAPK) signaling by PLX4032 is transient in thyroid and colorectal cancer cells. The rebound in extracellular signal-regulated kinase (ERK) in thyroid cells is accompanied by increased HER3 signaling caused by induction of ERBB3 (HER3) transcription through decreased promoter occupancy by the transcriptional repressors C-terminal binding protein 1 and 2 and by autocrine secretion of neuregulin-1 (NRG1). The HER kinase inhibitor lapatinib prevents MAPK rebound and sensitizes BRAF-mutant thyroid cancer cells to RAF or MAP-ERK kinase inhibitors. This provides a rationale for combining ERK pathway antagonists with inhibitors of feedback-reactivated HER signaling in this disease. The determinants of primary resistance to MAPK inhibitors vary between cancer types, due to preferential upregulation of specific receptor tyrosine kinases, and the abundance of their respective ligands.

| S-EPMC3651738 | biostudies-literature

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