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Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

ABSTRACT: Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

PROVIDER: PRJNA684750 | ENA |

REPOSITORIES: ENA

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Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

Project description:Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

| PRJNA522269 | ENA

Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

Project description:Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

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Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [tumors]

Project description:To investigate the mechanism underlying the effect of Brn2-loss we extracted mRNA from Braf-Pten-Brn2-wt, Braf-Pten-Brn2-het, and Braf-Pten-Brn2-hom mouse melanomas and performed microarray-based transcriptome analysis.

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Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2 [cell lines]

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Gene expression data from Tyr::CreErT2::BrafV600E Pten F/+ mouse tumors according to defloxing status of Brn2

Project description:This SuperSeries is composed of the SubSeries listed below.

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Modeling melanoma resistance in a genetically engineered mouse model

Project description:Melanoma is the deadliest type of skin cancer and its incidence is steadily increasing. Targeting melanoma cells posseses significant challenges due to primary or acquired therapy resistance in the majority of patients. Here, we describe the generation of an in vivo mouse model mimicking the key steps in melanoma initiation, progression and resistance acquisition. The well-characterized Tyr::CreERT2 BrafV600E Ptenfl/fl mouse model was used to induce melanoma initiation and subsequently therapy resistance to a combination of BRAF (PLX4720) and MEK (PD0325901) inhibitors. Our data reveal that all of the Tyr::CreERT2 BrafV600E Ptenfl/fl mice subjected to PLX4720+PD0325901 treatment ultimately developed resistance to these inhibitors. Introduction of genetic labelling by crossing Tyr::CreERT2 BrafV600E Ptenfl/fl mice with the TdTomato reporter allele allowed us not only to observe brain metastasis, which are rarely seen in this mouse model, but also to isolate metastatic melanoma cells using flow cytometry. The comparison of the expression profile of metastatic cells before and after resistance acquisition revealed a number of pathways significantly altered in resistant cells. Here, we describe and characterize a suitable mouse model to explore the molecular and cellular mechanisms of multiple stages of drug resistance in melanoma development. Finally, this experimental model might provide further understanding of the interplay between the immune system and melanoma cells.

2022-01-01 | GSE155537 | GEO

Optogenetic induction of Brn2 drive neural differentiation

Project description:We use optical induction of Brn2 to probe mechanisms for gating embryonic stem cell differentiation mRNA-seq time-course following Brn2 induciton

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BRN2 expression increases anoikis resistance in melanoma.

Project description:Melanoma tumors are highly heterogeneous, comprising of many cell populations that vary in their potential for growth and invasion. Differential transcription factor expression contributes to these phenotypic traits. BRN2, a member of the POU domain family of transcription factors is thought to play important roles in melanoma invasion and metastasis. However, how BRN2 functions during the metastatic process of melanoma remains largely unknown. We therefore investigated the effects of BRN2 expression in melanoma cells with no or low constitutive expression using a doxycycline-inducible system. Induction of BRN2 expression led to reduced proliferation and partial resistance to an inhibitor of mutated BRAF. Whole genome profiling analysis revealed novel targets and signaling pathway changes related to prevention of cell death induced by detachment from the extracellular matrix, known as anoikis resistance. Further investigation confirmed increased survival of BRN2 expressing cell lines in non-adherent conditions. Functionally, expression of BRN2 promoted induction of c-MET levels as well as increased phosphorylation of STAT3. Treatment with crizotinib, a c-MET inhibitor, decreased cellular viability of BRN2 expressing cells under non-adherent conditions to death by anoikis. These results highlight the importance of a largely overlooked transcription factor in the progression and metastasis of melanoma, and may suggest a strategy to target BRN2 expressing cells resistant to therapy and cell death by anoikis.

2020-02-25 | GSE145806 | GEO

Pigment producing melanocytes as the cells of origin of BRAFV600E-induced mouse cutaneous melanoma

Project description:To investigate whether cutaneous melanoma originates from a resident adult melanocyte stem cell (MSC) or a mature melanocyte, we created a model that recapitulates key histopathological features of human melanomagenesis by inducing a BRafV600E-driven melanomagenic program in interfollicular (IF) melanocytes located in mouse tails. To this end, we sequenced the transcriptome of FACS-sorted individual IFE reporter-positive cells from BRaf/Pten/tdTomato mice, the tails of which had been painted with 4-HT for 31 and 72 days, respectively. These time points were chosen as melanoma cells are exclusively found in the IF epidermis at day 31 (d31) and in both epidermis and dermis at day 72 (d72). Normal IF melanocytes from Tyr::CreERT2/+; ROSA26RLSL-tdTomato/+ were also isolated and profiled These data indicated that loss of differentiation markers occurs in a subset of targeted epidermal melanoma cells before the onset of dermal invasion and that this event may, at least partly, be a consequence of induction of Zeb1 expression.

2017-11-16 | GSE100607 | GEO

ChIP-Seq of Sox2 and Brn2 in ESCs, NPCs, and differentiating ESCs

Project description:We analyzed the genome-wide binding of Sox2 and POU factor partner factors, Oct4 in ESCs (using published datasets PMID:18692474 and GSM307137, GSM307154, GSM307155) and Brn2 in NPCs. We found that Sox2 and Oct4 co-occupied a large subset of promoters and enhancers in ESCs, but that Sox2 and Brn2 co-occupy predominantly enhancers. Further, we overexpressed Brn2 in differentiating ESCs and showed that ectopic Brn2 recruited Sox2 to NPC-specific targets, resulting in skewed differentiation towards the neural lineage. Examination of transcription factor binding in ESCs, NPCs, and differentiating ESCs by ChIP-Seq.

2013-02-20 | E-GEOD-35496 | biostudies-arrayexpress

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