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Homo sapiens strain:MIA PaCa-2 cells

ABSTRACT: RNA-seq analysis of cancer cells treated with LAT1 inhibitor or deprivation of valine or isoleucine

PROVIDER: PRJDB19590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR620246_1.fastq.gz	Fastqsanger.gz
	DRR620246_2.fastq.gz	Fastqsanger.gz
	DRR620247_1.fastq.gz	Fastqsanger.gz
	DRR620247_2.fastq.gz	Fastqsanger.gz
	DRR620248_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

MIA PaCa-2 cells treated with Gemcitabine

Project description:Pancreatic cancer cells (MIA PaCa-2) were treated with Gemcitabine and overall protein changes were studied

2022-09-15 | PXD030861 | Pride

Distinct translational profiles reveal elongation bottlenecks and codon-specific stalling during branched-chain amino acid deprivation [Ribo-Seq]

Project description:Cells regulate protein synthesis in response to fluctuating nutrient availability through highly coordinated mechanisms that affect both translation initiation and elongation. Branched-chain amino acids (BCAAs) - leucine, isoleucine, and valine - are essential nutrients with a significant impact on cellular physiology. However, how their simultaneous depletion affects the translational machinery and dynamics remains largely unclear. Here, we examine the immediate effects of short-term BCAA limitation on translational dynamics in mammalian cells. We performed RNA sequencing (RNA-seq) and ribosome profiling (Ribo-seq) on NIH3T3 cells subjected to single, double, or triple BCAA deprivation. Our analyses revealed increased ribosome dwell times in the deprived conditions, with especially strong stalling at all valine codons during valine and triple starvation, while leucine and isoleucine depletion triggered more moderate, codon-specific effects. Notably, isoleucine-specific stalling largely diminished under triple deprivation, likely due to early elongation bottlenecks at valine codons. Correlating these stalling events with tRNA charging levels revealed distinct tRNA isoacceptor regulation in each starvation condition. In addition, integrating proteome data showed that many proteins downregulated under BCAA deprivation harbor stalling sites, suggesting that compromised elongation contributes to decreased protein output. Together, these findings suggest that differential ribosome stalling under BCAA limitation reflects a balance between amino acid supply, tRNA charging dynamics, and stress pathway modulation, illustrating that codon usage biases can profoundly influence the global landscape of translation under nutrient stress.

2025-09-02 | GSE291653 | GEO

Distinct translational profiles reveal elongation bottlenecks and codon-specific stalling during branched-chain amino acid deprivation [RNA-Seq]

2025-09-02 | GSE291652 | GEO

Circular RNA expression signature of low-glucose-treated MIA PaCa-2 cells

Project description:Glucose metabolism makes contributions to the development of pancreatic ductal adenocarcinoma (PDAC). Meanwhile, circular RNAs, a subset of noncoding RNAs, plays an important role in glucose metabolism and cancer progression. Analysis of low-glucose-treated and normal-glucose-treated MIA PaCa-2 cells from 6 samples (3 samples each group) was conducted. Results indicate insight into molecular signature of the pathogenesis of PDAC in abberant glucose metabolism.

2019-10-20 | GSE121596 | GEO

Transcription profiling of Mia PaCa-2 cancer cells treated with a cell-permeable RAS inhibitor and its negative control

Project description:The action mechanism of a cell-permeable RAS inhibitor (Pen-cRaf-v1) and its binding-disrupting mutant (Pen-cRaf-v1-AA) was studied by transcription profiling of Mia PaCa-2 cancer cells treated with the inhibitors at the concentration of 10 microM for 3 hours.

2021-06-01 | E-MTAB-10403 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Control and rhCYGB treated in MIA PaCa-2 cell line

Project description:Purpose: The goal of this study is to investigate the inhibitor effect of Cytoglobin on pancreatic cancer Method: mRNA profiles of control and rhCYGB treated pancreatic cancer cells were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes and cell cycle regulated genes were down-regulated by the His-CYGB treatment.

2022-05-11 | GSE178358 | GEO

Effects of PGRMC1 phosphorylation status on MIA PaCa-2 cells

Project description:Progesterone Receptor Membrane Component 1 (PGRMC1) is expressed in many cancer cells, where it is associated with detrimental patient outcomes. Multiple different functions and cellular locations have been attributed to PGRMC1 in a variety of contexts, however the mechanisms underlying PGRMC1 biology remain obscure. The protein contains several phosphorylated residues including tyrosines which were acquired early in animal evolution and could be involved with animal cell differentiation mechanisms. Here we demonstrate that mutagenic manipulation of PGRMC1phosphorylation status in MIA PaCa-2 (MP) pancreatic cells exerts broad pleiotropic effects, influencing cell plasticity and tumorigenicity, as assayed by cell biological and proteomics measurements. Relative to MP cells over-expressing hemagglutinin (HA)-tagged wild-type PGRMC1- HA (WT), cells expressing a PGRMC1-HA-S57A/S181A double mutant (DM) exhibited reduced levels of proteins involved in energy metabolism and mitochondrial function. This was associated with Rho-kinase inhibitor (ROCKI)-sensitive changes including altered cell shape, motility, increased PI3K/Akt and JNK activity, and fragmented mitochondrial morphology. An S57A/Y180F/S181A triple mutant (TM) reduced PI3K/Akt and JNK activation, indicating involvement of Y180. Both TM cells and Y180F single mutant cells exhibited attenuated mouse xenograft tumor growth. Tyrosine 180 phosphorylation status of PGRMC1 exerts dramatic influence over cancer cell biology.

2020-03-03 | PXD014716 | Pride

mRNA expression data from RalGAPβ-deficient human pancreatic ductal adenocarcinoma cells (MIA PaCa-2), MIA PaCa-2 parental cells, and MIA PaCa-2 control cells

Project description:Pancreatic ductal adenocarcinoma, caused by activating mutation in K-Ras, is an aggressive malignancy due to its early invasion and matastasis. Ral GTPases, negatively regulated by RalGAP, are activated downstream of Ras and play a crucial role in development and progression of pancreatic ductal adenocarcinoma. However, the underlying mechanisms remain unclear. We used microarrays to detail the global programme of gene expression underlying the human pancreatic ductal adenocarcinoma cell line, MIA PaCa-2 with RalGAPβ deficiency or not, and identified distinct classes of Ral activation-related mRNA.

2023-04-24 | GSE223382 | GEO

Efficient Selection of Enhancers and Promoters from MIA PaCa-2 Pancreatic Cancer Cells by ChIP-lentiMPRA.

Project description:A library of active genome regulatory elements (putative promoters and enhancers) from MIA PaCa-2 pancreatic adenocarcinoma cells was constructed using a specially designed lentiviral vector and a massive parallel reporter assay (ChIP-lentiMPRA). Chromatin immunoprecipitation of the cell genomic DNA by H3K27ac antibodies was used for primary enrichment of the library for regulatory elements. Totally, 11,264 unique genome regions, many of which are capable of enhancing the expression of the CopGFP reporter gene from the minimal CMV promoter, were identified. The regions tend to be located near promoters. Based on the proximity assay, we found an enrichment of highly expressed genes among those associated with three or more mapped distal regions (2 kb distant from the 5'-ends of genes). It was shown significant enrichment of genes related to carcinogenesis or Mia PaCa-2 cell identity genes in this group. In contrast, genes associated with 1-2 distal regions or only with proximal regions (within 2 kbp of the 5'-ends of genes) are more often related to housekeeping functions. Thus, ChIP-lentiMPRA is a useful strategy for creating libraries of regulatory elements for the study of tumor-specific gene transcription.

| S-EPMC9740945 | biostudies-literature

Unraveling the CDK9/PP2A/ERK network in transcriptional pause release and complement activation in KRAS-mutant cancers (MIA PaCa-2 )

Project description:KRASG12C inhibitors (KRASG12Ci) AMG510 and MRTX849 have shown promising efficacy in clinical trials and been approved for the treatment of KRASG12C-mutant cancers. However, the emergence of therapy-related drug resistance limits their long-term potential. We measured gene expression using RNA-sequencing for pancreatic cancer cell line MIA PaCa-2 parental and their AMG510-resistant equivalent without treatment or treated with with G12C KRAS inhibitor AMG510.

2024-08-31 | GSE270796 | GEO

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