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ETV4 promotes metastasis in response to combined activation of PI3kinase and RAS signaling in a mouse model of advanced prostate cancer

ABSTRACT: Analysis of the transcriptome of mouse models of prostate cancer. NP (Nkx3.1CreERT2/+; Ptenfloxed/floxed) mice develop non-metastatic tumors while NPK (Nkx3.1CreERT2/+; Ptenfloxed/floxed; KrasG12D/+) mice develop metastatic tumors The NPK mice are also analyzed at early and late stages of tumorigenesis (1 vs. 3 months after induction)

ORGANISM(S): Mus musculus

PROVIDER: GSE47697 | GEO | 2013/07/23

SECONDARY ACCESSION(S): PRJNA207330

REPOSITORIES: GEO

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ETV4 promotes metastasis in response to combined activation of PI3kinase and RAS signaling in a mouse model of advanced prostate cancer

Project description:Analysis of the transcriptome of mouse models of prostate cancer. NP (Nkx3.1CreERT2/+; Ptenfloxed/floxed) mice develop non-metastatic tumors while NPK (Nkx3.1CreERT2/+; Ptenfloxed/floxed; KrasG12D/+) mice develop metastatic tumors The NPK mice are also analyzed at early and late stages of tumorigenesis (1 vs. 3 months after induction) Total RNA obtained from prostate tumors of different genotypes and at different stages of dissease as indicated

2013-07-23 | E-GEOD-47697 | biostudies-arrayexpress

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Project description:Single-cell transcriptome analysis of lineage-marked prostate primary tumors and metastases from the NPK mouse model (Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+; R26R-CAG-LSL-EYFP/+)

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Predicting drug response in human prostate cancer from preclinical analysis of in vivo mouse models (II)

Project description:Analysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis.

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2015-09-17 | E-GEOD-69213 | biostudies-arrayexpress

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2015-09-17 | GSE69211 | GEO

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2015-09-17 | E-GEOD-69211 | biostudies-arrayexpress

Translation control of the immune checkpoint in cancer and its therapeutic targeting

Project description:Cancer cells develop mechanisms to escape immunosurveillance, among which modulating the expression of immune suppressive messenger RNAs is most well-documented. However, how this is molecularly achieved remains largely unresolved. Here, we develop an in vivo mouse model of liver cancer to study oncogene cooperation in immunosurveillance. We show that MYC overexpression (MYCTg) synergizes with KRASG12D to induce an aggressive liver tumor leading to metastasis formation and reduced mouse survival compared with KRASG12D alone. Genome-wide ribosomal footprinting of MYCTg;KRASG12 tumors compared with KRASG12D revealed potential alterations in translation of mRNAs, including programmed-death-ligand 1 (PD-L1). Further analysis revealed that PD-L1 translation is repressed in KRASG12D tumors by functional, non-canonical upstream open reading frames in its 5′ untranslated region, which is bypassed in MYCTg;KRASG12D tumors to evade immune attack. We show that this mechanism of PD-L1 translational upregulation was effectively targeted by a potent, clinical compound that inhibits eIF4E phosphorylation, eFT508, which reverses the aggressive and metastatic characteristics of MYCTg;KRASG12D tumors. Together, these studies reveal how immune-checkpoint proteins are manipulated by distinct oncogenes at the level of mRNA translation, which can be exploited for new immunotherapies.

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