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ADRA2A is a suppressor of the basal-like/squamous subtype and reduces disease aggressiveness of pancreatic cancer

ABSTRACT: ADRA2A is a suppressor of the basal-like/squamous subtype and reduces disease aggressiveness of pancreatic cancer

PROVIDER: PRJNA1081404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28125642_1.fastq.gz	Fastqsanger.gz
	SRR28125642_2.fastq.gz	Fastqsanger.gz
	SRR28125643_1.fastq.gz	Fastqsanger.gz
	SRR28125643_2.fastq.gz	Fastqsanger.gz
	SRR28125644_1.fastq.gz	Fastqsanger.gz

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ADRA2A is a suppressor of the basal-like/squamous subtype and reduces disease aggressiveness of pancreatic cancer

Project description:Pancreatic cancer is a heterogeneous disease and consists of distinct subtypes. Here, we investigated candidate suppressor genes of the basal-like/squamous subtype, a more aggressive molecular subtype of pancreatic ductal adenocarcinoma (PDAC). Through an integrated transcriptome analysis, we identified the ADRA2A, as being downregulated in the basal-like/squamous PDAC using a discovery and validation approach. ADRA2A downregulation is associated with decreased patient survival. The goal of this study was to identify ADRA2A-induced molecular signatures in PDAC.

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LMO3 is a suppressor of the basal-like/squamous PDAC subtype and reduces disease aggressiveness of pancreatic cancer through glycerol 3-phosphate metabolism

Project description:Pancreatic cancer is a heterogenous disease and consists of distinct subtypes. Here, we searched for candidate suppressor genes of the basal-like/squamous subtype, a more aggressive molecular subtype of pancreatic ductal adenocarcinoma (PDAC). Through an integrated transcriptome analysis, we identified the LMO3, as being downregulated in the basal-like/squamous PDAC using a discovery and validation approach. LMO3 downregulation associated with decreased patient survival. The goal of this study was aimed to identify LMO3 induced molecular signatures in PDAC.

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<scp>ELAPOR1</scp> induces the classical/progenitor subtype and contributes to reduced disease aggressiveness through metabolic reprogramming in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a heterogeneous disease with distinct molecular subtypes described as classical/progenitor and basal-like/squamous PDAC. We hypothesized that integrative transcriptome and metabolome approaches can identify candidate genes whose inactivation contributes to the development of the aggressive basal-like/squamous subtype. Using our integrated approach, we identified endosome-lysosome associated apoptosis and autophagy regulator 1 (ELAPOR1/KIAA1324) as a candidate tumor suppressor in both our NCI-UMD-German cohort and additional validation cohorts. Diminished ELAPOR1 expression was linked to high histological grade, advanced disease stage, the basal-like/squamous subtype, and reduced patient survival in PDAC. In vitro experiments demonstrated that ELAPOR1 transgene expression not only inhibited the migration and invasion of PDAC cells but also induced gene expression characteristics associated with the classical/progenitor subtype. Metabolome analysis of patient tumors and PDAC cells revealed a metabolic program associated with both upregulated ELAPOR1 and the classical/progenitor subtype, encompassing upregulated lipogenesis and downregulated amino acid metabolism. 1-Methylnicotinamide, a known oncometabolite derived from S-adenosylmethionine, was inversely associated with ELAPOR1 expression and promoted migration and invasion of PDAC cells in vitro. Taken together, our data suggest that enhanced ELAPOR1 expression promotes transcriptome and metabolome characteristics that are indicative of the classical/progenitor subtype, whereas its reduction associates with basal-like/squamous tumors with increased disease aggressiveness in PDAC patients. These findings position ELAPOR1 as a promising candidate for diagnostic and therapeutic targeting in PDAC.

2024-04-02 | MTBLS9418 | MetaboLights

LMO3 is a suppressor of the basal-like/squamous PDAC subtype and reduces disease aggressiveness of pancreatic cancer through glycerol 3-phosphate metabolism

Project description:LMO3 is a suppressor of the basal-like/squamous PDAC subtype and reduces disease aggressiveness of pancreatic cancer through glycerol 3-phosphate metabolism

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ELAPOR1 induces the classical/progenitor subtype and contributes to reduced disease aggressiveness through metabolic reprogramming in pancreatic cancer

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Correlation of global micro RNA expression with basal cell carcinoma subtype

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Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines

2016-08-11 | E-GEOD-72009 | biostudies-arrayexpress

The RNA binding protein QKI guides a pro-mesenchymal splicing program driving a subtype switch and limiting outcome in pancreatic cancer [PANC-1 and HPAF-II]

Project description:Transcriptomic analyses have identified two molecular PDAC subtypes, one of which, namely basal-like subtype, is associated with chemoresistance and worse clinical outcomes. Splicing dysregulation is known to contribute to PDAC malignancy. Functional studies in PDAC cells lines identified the splicing factor QKI as a key determinant of a basal-like splicing signature associated with increased tumor aggressiveness. Our studies demonstrate that QKI represses splicing events associated with the classical subtype and improved clinical outcome, while promoting basal-like events associated with shorter survival.

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Over-expression of miR-146a in basal-like breast cancer cells confers enhanced tumorigenic potential in association with altered p53 status

Project description:The tumor suppressor p53 is the most frequently mutated gene in human cancers, mutated in 25-30% of breast cancers. However, mutation rates differ according to breast cancer subtype, being more prevalent in aggressive estrogen receptor (ER) negative tumors, basal-like and HER2 amplified subtypes. This heterogeneity suggests that p53 may function differently across breast cancer subtypes. We used RNAi-mediated p53 knockdown (KD) and antagomir-mediated KD of microRNAs to study how gene expression and cellular response to p53 loss differ in luminal vs. basal-like breast cancer. As expected, p53 loss caused down regulation of established p53 targets (e.g. p21 and miR-34 family) and increased proliferation in both luminal and basal-like cell lines. However, some p53-dependent changes were subtype-specific, including expression of miR-134, miR-146a, and miR-181b. To study the cellular response to miR-146a upregulation in p53-impaired basal-like lines, antagomir knockdown of miR-146a was performed. KD of miR-146a caused decreased proliferation and increased apoptosis, effectively ablating the effects of p53 loss. Furthermore, we found that miR-146a upregulation decreased NF-kB expression and downregulated the NF-kB-dependent extrinsic apoptotic pathway (including TNF, FADD, and TRADD) and antagomir-mediated miR-146a KD restored expression of these components, suggesting a plausible mechanism for miR-146a-dependent cellular responses. These findings are relevant to human basal-like tumor progression in vivo, since miR-146a is highly expressed in p53-mutant basal-like breast cancers. These findings suggest that targeting miR-146a expression may have value for altering the aggressiveness of p53 mutant basal-like tumors. reference x sample

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