xCT knockdown in human breast cancer cells delays onset of cancer-induced bone pain.

Molecular Pain
Robert G UngardGurmit Singh

Abstract

Cancers in the bone produce a number of severe symptoms including pain that compromises patient functional status, quality of life, and survival. The source of this pain is multifaceted and includes factors secreted from tumor cells. Malignant cells release the neurotransmitter and cell-signaling molecule glutamate via the oxidative stress-related cystine/glutamate antiporter, system xC-, which reciprocally imports cystine for synthesis of glutathione and the cystine/cysteine redox cycle. Pharmacological inhibition of system xC- has shown success in reducing and delaying the onset of cancer pain-related behavior in mouse models. This investigation describes the development of a stable siRNA-induced knockdown of the functional trans-membrane system xC- subunit xCT ( SLC7A11) in the human breast cancer cell line MDA-MB-231. Clones were verified for xCT knockdown at the transcript, protein, and functional levels. RNAseq was performed on a representative clone to comprehensively examine the transcriptional cellular signature in response to xCT knockdown, identifying multiple differentially regulated factors relevant to cancer pain including nerve growth factor, interleukin-1, and colony-stimulating factor-1. Mice were inoculated in...Continue Reading

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Citations

Feb 28, 2020·Canadian Journal of Pain = Revue Canadienne De La Douleur·Robert G UngardGurmit Singh

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Methods Mentioned

BETA
RNAseq
electrophoresis
Assay
xenograft
reverse transcription PCR
X-ray

Software Mentioned

CummeRbund for RStudio
GraphPad
Cufflinks
DWB
FastQC
Galaxy
Bioconductor
Cuffmerge
DAVID
Tophat

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