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PANC-1 and AsPC-1 human pancreatic carcinoma cells under hypoxia, nutrient starvation and low pH culture condition

ABSTRACT: PANC-1 and AsPC-1 human pancreatic carcinoma cells under hypoxia, nutrient starvation and low pH culture condition

PROVIDER: PRJNA363006 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5196800.fastq.gz	Fastqsanger.gz
	SRR5196830_1.fastq.gz	Fastqsanger.gz
	SRR5196830_2.fastq.gz	Fastqsanger.gz
	SRR5196801.fastq.gz	Fastqsanger.gz
	SRR5196802.fastq.gz	Fastqsanger.gz

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Gene expression in PANC-1 and AsPC-1 human pancreatic carcinoma cells under hypoxia, nutrient starvation and low pH culture condition.

Project description:The conditions of the tumor microenvironment, such as hypoxia and nutrient starvation, play critical roles in cancer progression. However, the role of acidic extracellular pH in cancer progression is not studied as extensively as that of hypoxia. Here, we show that extracellular acidic pH (pH 6.8) triggered activation of sterol regulatory element-binding protein 2 (SREBP2) by stimulating nuclear translocation and promoter binding to its targets along with intracellular acidification. Interestingly, inhibition of SREBP2, but not SREBP1, suppressed the upregulation of low pH-induced cholesterol biosynthesis-related genes. Moreover, acyl-CoA synthetase short-chain family member 2 (ACSS2), a direct SREBP2 target, provided a growth advantage to cancer cells under acidic pH. Furthermore, acidic pH-responsive SREBP2 target genes were associated with reduced overall survival of cancer patients. Thus, our findings show that SREBP2 is a key transcriptional regulator of metabolic genes and progression of cancer cells, partly in response to extracellular acidification.

2017-01-25 | GSE93988 | GEO

Open chromatin region, histone acetylation, and SREBP2 binding in PANC-1 and AsPC-1 human pancreatic carcinoma cells under hypoxia, nutrient starvation and low pH culture condition.

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PANC-1 and AsPC-1 human pancreatic carcinoma cells under hypoxia, nutrient starvation and low pH culture condition

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Project description:Purpose: It is increasingly appreciated that intracellular pH changes are important biological signals. This motivates the elucidation of molecular mechanisms of pH-sensing. We determined that a nucleocytoplasmic pH oscillation was required for the transcriptional response to carbon starvation in S. cerevisiae. Methods: We performed RNA sequencing analysis to determine the extent of the requirement for theSNF5 QLC in the activation of glucose-repressed genes. Total RNA was extracted from WT, ΔQ-snf5 and HtoA-snf5 strains during exponentially growth (+Glu) and after 4 hours of glucose starvation. Next, Poly-A selection was performed using Dynabeads and libraries were performed following manufactures indications. Sequencing of the 32 samples was performed on an Illumina Hi-seq on two lanes. RNA-seq data were aligned to the University of California, Santa Cruz (UCSC), sacCer2 genome using Kallisto (0.43.0,http://www.nature.com/nbt/journal/v34/n5/full/nbt.3519.html) and downstream visualization and analysis was done using R (3.2.2). Differential gene expression analysis, heat maps and volcano plots were created using DESeq2 where a wald test was used to determine differentially expressed genes and Euclidean distance to calculate clustering for heat maps. Conclusions: We found that pH changes and the SNF5 QLC are required for correct transcriptional reprogramming upon carbon starvation, but the dependencies are nuanced.

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Loss of major nutrient sensing and signaling pathways suppresses starvation lethality in electron transport chain mutants (DenseTimeCourse)

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