Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis

ABSTRACT: DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis

PROVIDER: PRJNA510109 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8320980_1.fastq.gz	Fastqsanger.gz
	SRR8320980_2.fastq.gz	Fastqsanger.gz
	SRR8320981_1.fastq.gz	Fastqsanger.gz
	SRR8320981_2.fastq.gz	Fastqsanger.gz
	SRR8320982_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis

Project description:Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid–binding protein 1. However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that the RNA-binding protein DDX5 binds to the mRNA transcripts of C3 and fatty acid–binding protein 1 to augment their expressions posttranscriptionally. Knocking out DDX5 in epithelial cells protected mice from intestinal tumorigenesis and dextran sodium sulfate–induced col- itis. Identification of DDX5 as a common upstream regulator of tissue-specific oncogenic molecules provides an excellent therapeutic target for intestinal diseases.

2020-08-14 | GSE123881 | GEO

DDX5 targets tissue specific RNAs to promote intestine tumorigenesis

Project description:Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid-binding protein 1 (FABP1). However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that an RNA binding protein DDX5 augments C3 and FABP1 expressions post-transcriptionally to promote tumorigenesis in the colon and small intestine, respectively. Mice with epithelial-specific knockout of DDX5 are protected from intestine tumorigenesis. The identification of DDX5 as the common upstream regulator of tissue-specific oncogenic molecules provides a new therapeutic target for intestine cancers.

2020-08-12 | GSE124023 | GEO

DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis.

Project description:Tumorigenesis in different segments of the intestinal tract involves tissue-specific oncogenic drivers. In the colon, complement component 3 (C3) activation is a major contributor to inflammation and malignancies. By contrast, tumorigenesis in the small intestine involves fatty acid-binding protein 1 (FABP1). However, little is known of the upstream mechanisms driving their expressions in different segments of the intestinal tract. Here, we report that the RNA-binding protein DDX5 binds to the mRNA transcripts of C3 and Fabp1 to augment their expressions posttranscriptionally. Knocking out DDX5 in epithelial cells protected mice from intestinal tumorigenesis and dextran sodium sulfate (DSS)-induced colitis. Identification of DDX5 as a common upstream regulator of tissue-specific oncogenic molecules provides an excellent therapeutic target for intestinal diseases.

| S-EPMC7441524 | biostudies-literature

Engineered extrachromosomal oncogene amplifications promote tumorigenesis

Project description:Engineered extrachromosomal oncogene amplifications promote tumorigenesis

| PRJNA1100533 | ENA

DDX5 in colonic tumors

Project description:The Asp-Glu-Ala-Asp (DEAD)-box RNA binding protein, DDX5, is ubiquitously expressed in many cell types, yet its role in RNA metabolism and its downstream function in vivo has not been fully elucidated. In the intestine, DDX5 is highly expressed in the intestinal epithelial cell (IECs) and contributes to tumorigenesis. Here, we used a conditional mouse lines where DDX5 is knocked out in IECs upon Tamoxifen administration to uncover mechanisms underlying DDX5 functions in colon tumors.

2021-12-03 | GSE146014 | GEO

DDX5 targets tissue specific RNAs to promote intestine tumorigenesis

Project description:DDX5 targets tissue specific RNAs to promote intestine tumorigenesis

| PRJNA510585 | ENA

Engineered extrachromosomal oncogene amplifications promote tumorigenesis (RNA-Seq)

Project description:Engineered extrachromosomal oncogene amplifications promote tumorigenesis (RNA-Seq)

| PRJNA1100544 | ENA

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.

Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability. Examination of Prep1 and Meis1 in three cell type

2014-03-05 | E-GEOD-54221 | biostudies-arrayexpress

Modeling cellular pliancy-dependent oncogene-induced signaling and chemotherapeutic response during breast tumorigenesis

Project description:Modeling cellular pliancy-dependent oncogene-induced signaling and chemotherapeutic response during breast tumorigenesis

2021-06-30 | GSE153216 | GEO

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis [hP]

2016-06-01 | E-GEOD-58802 | biostudies-arrayexpress