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Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

ABSTRACT: MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE126143 | GEO | 2019/12/26

REPOSITORIES: GEO

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Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

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RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

Project description:In this study we identified genes regulated by CASZ1b in SMS-CTR cells

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RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

Project description:RNA-sequencing analysis to investigate genes regulated by CASZ1 in SMS-CTR cells

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Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

Project description:In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.

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Efficacy of trametinib and dabrafenib associated with radioactive iodine for the treatment of refractory metastatic differentiated thyroid cancer

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2023-09-01 | E-MTAB-12837 | biostudies-arrayexpress

Efficacy of trametinib and dabrafenib associated with radioactive iodine for the treatment of refractory metastatic differentiated thyroid cancer (KRAS cohort)

Project description:Efficacy of a selective MEK (trametinib) and BRAFV600E (dabrafenib) inhibitors associated with radioactive iodine (RAI) for the treatment of refractory metastatic differentiated thyroid cancer with RAS (current cohort) or BRAFV600E mutation. To evaluate the objective response rate according to RECIST criteria in thyroid cancer patients with metastatic radioactive iodine (RAI) refractory disease, 6 months after a treatment combining in each arm of the phase II trial (patients with RAS mutation or patients with BRAFV600E mutation): - Arm A: 6 weeks of trametinib followed by RAI treatment (5.5 GBq following rhTSH) in patients with RAS mutation - Arm B: 6 weeks of trametinib plus dabrafenib followed by RAI treatment (5.5 GBq following rhTSH) in patients with BRAFV600E mutation

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CASZ1 is essential for activation of epidermal terminal differentiation

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Capicua-dependent transcriptional changes in human cancer cell lines treated with trametinib

Project description:We performed a genome-scale CRISPR screen in a KRAS-mutant pancreatic cancer cell line treated with the MEK inhibitor trametinib, and found that loss of the transcriptional repressor CIC confers resistance to MEK inhibition. We determined that CIC loss also confers resistance to MEK or BRAF inhibition in lung cancer, colorectal cancer, and melanoma cell lines with mutant RAS or BRAF. CIC is a transcriptional repressor that is phosphorylated and inhibited by the MAPK pathway. We hypothesized that inhibition of the MAPK pathway would lead to activation of CIC and repression of CIC target genes. Loss of CIC would therefore restore expression of these genes, conferring drug resistance. To identify the relevant CIC target genes that mediate trametinib resistace, we generated 4 Cas9-expressing cell lines from different lineages and with different RAS or RAF mutations, and generated control (gGFP) or CIC-knockout (gCIC) cell lines. We treated cells with DMSO or trametinib for 24 hours, and performed NRA-seq. We found that trametinib treatment reduces expression of at least one member of the PEA3 family of ETS transcription factors (ETV1, ETV4, and ETV5) in all cell lines assessed, and that loss of CIC results in maintained expression of these genes despite MEK inhibition. We further validated that ETV1, 4, and 5 expression was necessary for resistance mediated by CIC loss; and that ETV1, 4, or 5 expression was sufficient to confer trametinib resistance.

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