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Transcriptome and chromatin changes during CRC organoid outgrowth as proxy for metastatic outgrowth

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE207071 | GEO | 2023/12/01

REPOSITORIES: GEO

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Transcriptome and chromatin changes during CRC organoid outgrowth as proxy for metastatic outgrowth [bulkATACseq_AKPS]

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Transcriptome and chromatin changes during CRC organoid outgrowth as proxy for metastatic outgrowth

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Autophagic Degradation of NBR1 Restricts Metastatic Outgrowth during Mammary Tumor Progression.

Project description:Although autophagy is being pursued as a therapeutic target in clinical oncology trials, its effects on metastasis, the principal cause of cancer mortality, remain unclear. Here, we utilize mammary cancer models to temporally delete essential autophagy regulators during carcinoma progression. Though genetic ablation of autophagy strongly attenuates primary mammary tumor growth, impaired autophagy promotes spontaneous metastasis and enables the outgrowth of disseminated tumor cells into overt macro-metastases. Transcriptomic analysis reveals that autophagy deficiency elicits a subpopulation of otherwise luminal tumor cells exhibiting basal differentiation traits, which is reversed upon preventing accumulation of the autophagy cargo receptor, Neighbor to BRCA1 (NBR1). Furthermore, pharmacological and genetic induction of autophagy suppresses pro-metastatic differentiation and metastatic outgrowth. Analysis of human breast cancer data reveal that autophagy gene expression inversely correlates with pro-metastatic differentiation signatures and predicts overall and distant metastasis-free survival. Overall, these findings highlight autophagy-dependent control of NBR1 as a key determinant of metastatic progression.

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Transcriptome analysis during axillary shoot outgrowth

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Transcriptome analysis during axillary shoot outgrowth

Project description:In plant axillary bud dormancy and outgrowth are regulated by phytohoromones, but it is still unknown about its molecular mechanism. We reveal that Arabidopsis axillary buds located at axil of rosette leaves show dormancy and that this is broken by the decapitation of main stem, resulting in the bud outgrowth. To investigate about the molecular mechanisms of dormancy and outgrowth, we carried out gene expression analysis during axillary shoot outgrowth in Arabidopsis wild type Columbia accession. Since axillary buds did not initiate outgrowth (dormancy) at 5 day after bolting of main stem, we used 5-day bolted plants as a control (before decapitation). Then, main stems were decapitated, and axillary shoots were collected at 24 hours after decapitation (named as growing shoot). Total RNA was prepared from either control or growing shoots and used for the microarray analysis. We carried out duplicate microarray analysis using independent plant materials.Ref):Tatematsu et al., Plant Physiol. 138: 757-766 (2005). Keywords: Expression profilling by array

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