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PAX5 controls lineage transitions between neuroendocrine and non-neuroendocrine states during carcinoma progression

ABSTRACT: PAX5 controls lineage transitions between neuroendocrine and non-neuroendocrine states during carcinoma progression

PROVIDER: PRJNA689218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13342017_1.fastq.gz	Fastqsanger.gz
	SRR13342017_2.fastq.gz	Fastqsanger.gz
	SRR13342018_1.fastq.gz	Fastqsanger.gz
	SRR13342018_2.fastq.gz	Fastqsanger.gz
	SRR13342019_1.fastq.gz	Fastqsanger.gz

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Lineage specific chromatin modification guides Pax5 mediated gene expression in neuroendocrine like differentiation of prostate cancer (ChIP-Seq)

Project description:Neuroendocrine-like differentiation of castration-resistant prostate cancer is highly aggressive and independent of the androgen receptor signaling for its progression. During such lineage differentiation, adenocarcinoma adopts basal and neuronal characteristics that alter its clinical progression, limiting its therapeutic opportunities. Inadequate understanding of the molecular mechanism for such transformation also restricts its targeted therapies. Using ATAC-Seq, acetylated-histone ChIP-seq, and RNA-seq, we have characterized the early transformation process and identified chromatin occupancy and gene expression differences between adenocarcinoma and neuroendocrine-like cancer cells. By comparing differentially active promoter signatures during lineage-specific transcriptional events, our results indicate that the transcription factor Pax5 plays a major role in the trans-differentiation processes. Using LuCaP PDX tissues and metastatic prostate cancer TMA, in conjunction with patient RNA-expression databases, we validated that Pax5 is selectively expressed only in neuroendocrine like cancer but not in adenocarcinoma. Further analysis reveals that Pax5 expression is involved in neuronal gene expression and critical for imparting therapy resistance. Further, our results indicate that increased hydroxymethylation at the Pax5 promoter leads to recruitment of the homeobox transcription factor Pbx1 for Pax5 transcription. This is in line with our findings that lineage-specific expression of Pbx1/Pax5 is associated with the development of neuroendocrine-like differentiation. Our study suggests, upon continuous exposure to anti-androgen therapeutic stress, chromatin modifications are associated with Pax5-mediated gene expression to adopt neuroendocrine-like characteristics of advanced prostate cancer.

2024-07-25 | GSE210846 | GEO

Lineage specific chromatin modification guides Pax5 mediated gene expression in neuroendocrine like differentiation of prostate cancer (ATAC-Seq)

2024-07-25 | GSE210844 | GEO

Lineage specific chromatin modification guides Pax5 mediated gene expression in neuroendocrine like differentiation of prostate cancer (RNA-Seq)

2024-07-25 | GSE210847 | GEO

PAX5 promotes progression of neuroendocrine prostate cancer

Project description:PAX5 promotes progression of neuroendocrine prostate cancer

| PRJNA533095 | ENA

PAX5 controls lineage transitions between neuroendocrine and non-neuroendocrine states during carcinoma progression

Project description:Single cell lung suspensions of SCLC tissues were generated. scRNA-seq was performed on CD45 and CD31 negative live cells sorted by FACS. Purified cells were clustered to evaluate the cancer cell sub-clusters.

2022-12-18 | GSE164145 | GEO

A SIRT7-dependent acetylation switch regulates early B-cell differentiation and lineage commitment through PAX5

Project description:B lymphopoiesis is a key developmental event orchestrated by a complex combinatorial action of lineage-specific transcription factors. In early B cell progenitors, lineage commitment is directly mediated by the master regulator PAX5, whose deficiency is commonly associated with B cell Acute Lymphoblastic Leukemia (B-ALL). Despite its essential role in mammalian immunity, the regulatory mechanisms that control PAX5 function remain largely unknown. Here we show that NAD+-dependent enzyme SIRT7 coordinates B cell development progression through PAX5. We have identified a SIRT7-dependent regulatory switch based on dynamic deacetylation of a single PAX5 residue, which controls its activity and thereby B cell fate. While a PAX5K198 acetylated mimic is incapable of inducing both B cell development and identity due to reduced protein stability and impaired binding to chromatin, deacetylation of this residue boosts PAX5 activity, leading to massive gene repression and in vivo restoration of B cell commitment but not differentiation. These findings suggest an unexpected uncoupling of hematopoietic differentiation and lineage commitment. Further supporting the functional relevance of the SIRT7-PAX5 axis, the interplay between both factors is conserved in human B-ALL, where high SIRT7 expression is an independent good prognostic factor. Our findings unveil a crucial mechanism in the regulation of B cell production based on the control of PAX5 function and underscore the key role of Sirtuins in the regulation of the immune system.

2024-09-20 | PXD046457 | Pride

PAX5 promotes progression of neuroendocrine prostate cancer

Project description:Analysis of prostate adnocarcinoma cell line LNCaP cells overexpression pair box 5 (PAX5) for up to 4 days. The goals of this study are to compare PAX5 overexpression in LNCaP cell drives transcriptome profiling (RNA-seq) changes.

2021-01-31 | GSE129887 | GEO

PAX5 promotes heterocharomatin formation

Project description:Heterochromatin has a high density of DNA and low rates of gene transcription.H3k9me3 is a conserved histone modification, and is best known for its role in constitutive heterochromatin formation.H1155, which is a neuroendocrine large cell lung cancer cell line, has a dense nucleus and a high level of occupancy of H3K9me3. PAX5 is a neurogenesis and B lymphocyte development transcription factor, and endogenous expressed in neuroendocrine carcinoma, including H1155 cell line. To assess whether PAX5 promotes heterochromatin formation in H1155, we knock out PAX5 in H1155 cell (KO-PAX5) by CRISPR/Cas9 and use H3K9me3 to performed ChIP-seq.

2024-01-17 | GSE165035 | GEO

Lineage specific chromatin modification guides Pax5 mediated gene expression in neuroendocrine like differentiation of prostate cancer

Project description:Lineage specific chromatin modification guides Pax5 mediated gene expression in neuroendocrine like differentiation of prostate cancer

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Essential role of the Pax5 C-terminal domain in controlling B cell commitment and development

Project description:Pax5 controls B-cell commitment, development and immunity by repressing B-lineage-inappropriate genes and activating B-cell-specific genes. In addition to the N-terminal DNA-binding paired domain, Pax5 contains a conserved octapeptide, partial homeodomain and C-terminal sequences with transactivating and inhibitory potential. To understand how the C-terminal domains of Pax5 contribute to the repression and activation function of Pax5, we performed Pax5 pulldown combined with mass spectrometry to identify coactivator or corepressor complexes that bind to the C-terminal regions of Pax5.

2023-08-24 | PXD040424 | Pride

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