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Series GSE249082 Query DataSets for GSE249082
Status Public on Dec 03, 2023
Title SERS analysis of cancer cell-secreted purines reveals a unique paracrine crosstalk in MTAP-deficient tumors
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary The tumor microenvironment (TME) is a dynamic pseudoorgan that shapes the development and progression of cancers. It is a complex ecosystem shaped by interactions between tumor and stromal cells. Although the traditional focus has been on the paracrine communication mediated by protein messengers, recent attention has turned to the metabolic secretome in tumors. Metabolic enzymes, together with exchanged substrates and products, have emerged as potential biomarkers and therapeutic targets. However, traditional techniques for profiling secreted metabolites in complex cellular contexts are limited. Surface-enhanced Raman scattering (SERS) has emerged as a promising alternative due to its nontargeted nature and simplicity of operation. Although SERS has demonstrated its potential for detecting metabolites in biological settings, its application in deciphering metabolic interactions within multicellular systems like the TME remains underexplored. In this study, we introduce a SERS-based strategy to investigate the secreted purine metabolites of tumor cells lacking methylthioadenosine phosphorylase (MTAP), a common genetic event associated with poor prognosis in various cancers. Our SERS analysis reveals that MTAP-deficient cancer cells selectively produce methylthioadenosine (MTA), which is taken up and metabolized by fibroblasts. Fibroblasts exposed to MTA exhibit: i) molecular reprogramming compatible with cancer aggressiveness, ii) a significant production of purine derivatives that could be readily recycled by cancer cells, and iii) the capacity to secrete purine derivatives that induce macrophage polarization. Our study supports the potential of SERS for cancer metabolism research and reveals an unprecedented paracrine crosstalk that explains TME reprogramming in MTAP-deleted cancers.
 
Overall design HBF in control conditions vs HBF treated with MTA to resemble the phenotype in MTAP -/- Tumors.
 
Contributor(s) Valera PS, Plou J, García I, Astobiza I, Viera C, Sasselli IR, Carracedo A, Liz-Marzán LM, Aransay AM
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Submission date Nov 30, 2023
Last update date Dec 03, 2023
Contact name Ana Maria Aransay
E-mail(s) amaransay@cicbiogune.es
Phone 0034944061325
Organization name CIC bioGUNE
Department Genome Analysis Platform
Street address Parque tecnologico de Bizkaia, Building 801-A
City Derio
State/province BIZKAIA
ZIP/Postal code 48160
Country Spain
 
Platforms (1)
GPL24676 Illumina NovaSeq 6000 (Homo sapiens)
Samples (8)
GSM7926096 Control, Breast Fibroblasts, rep1
GSM7926097 Control, Breast Fibroblasts, rep2
GSM7926098 Control, Breast Fibroblasts, rep3
Relations
BioProject PRJNA1047127

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE249082_AC-59_RawCounts.txt.gz 5.3 Mb (ftp)(http) TXT
SRA Run SelectorHelp
Raw data are available in SRA

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