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Distinct immune microenvironments between primary and paired metastatic tumors in gastric cancer patients

ABSTRACT: We performed RNA-seq to investigate the differences in the gene expression profiles between primary gastric cancer (PGC) and paired metastatic gastric cancer (MGC). RNA-sequencing was performed on 7 paired PGC and MGC FFPE tissues. The transcriptome profiling of the two groups (MGC vs PGC) including immune response gene signature was analyzed. Total RNA was isolated using Trizol reagent. Extracted RNA samples were processed using the QuantSeq 3’mRNA-Seq Library Prep Kit and sequenced on an Illumina NextSeq 500. QuantSeq 3’mRNA-Seq reads were aligned using Bowtie2. The alignment file was used to assemble transcripts and the Read Count data was processed based on quantile normalization method using EdgeR within R. We identified 519 differentially regulated genes between the two sets, 76 of which were significantly up-regulated and 443 significantly down-regulated in MGCs. Among DEGs, 33 immune response genes were selected using QuickGO database (https://www.ebi.ac.uk/QuickGO/), with majority (27/33) of them exhibiting downregulation in the MGC samples. In summary, RNA sequencing data revealed that immune-related gene expression were down-regulated in MGC compared to PGC. We performed RNA-seq to investigate the differences in the gene expression profiles between primary gastric cancer (PGC) and paired metastatic gastric cancer (MGC). RNA-sequencing was performed on 7 paired PGC and MGC FFPE tissues. The transcriptome profiling of the two groups (MGC vs PGC) including immune response gene signature was analyzed. Total RNA was isolated using Trizol reagent. Extracted RNA samples were processed using the QuantSeq 3’mRNA-Seq Library Prep Kit and sequenced on an Illumina NextSeq 500. QuantSeq 3’mRNA-Seq reads were aligned using Bowtie2. The alignment file was used to assemble transcripts and the Read Count data was processed based on quantile normalization method using EdgeR within R. We identified 519 differentially regulated genes between the two sets, 76 of which were significantly up-regulated and 443 significantly down-regulated in MGCs. Among DEGs, 33 immune response genes were selected using QuickGO database (https://www.ebi.ac.uk/QuickGO/), with majority (27/33) of them exhibiting downregulation in the MGC samples. In summary, RNA sequencing data revealed that immune-related gene expression were down-regulated in MGC compared to PGC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147043 | GEO | 2020/03/16

REPOSITORIES: GEO

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Project description:Background & Aims: Metaplasia and dysplasia in the corpus are reportedly derived from dedifferentiation of chief cells. However, the cellular origin of metaplasia and cancer remained uncertain. Therefore, we investigated whether pepsinogen Ctranscript expressing cells (PGC-transcript expressing cells) represent the cellular origin of metaplasia and cancer using a novel Pgc-specific CreERT2 recombinase mouse model. Methods: We generated a Pgc-mCherry-IRES-CreERT2 (Pgc-CreERT2) knock-in mouse model. Pgc-CreERT2/+ and Rosa-EYFP mice were crossed to generate PgcCreERT2/Rosa-EYFP (Pgc-CreERT2/YFP) mice. Gastric tissues were collected, followed by lineage-tracing experiments, histological and immunofluorescence staining. We further established Pgc-CreERT2;Kras G12D/+ mice and investigated whether PGCtranscript expressing cells are responsible for the precancerous state in gastric glands. To investigate cancer development from PGC-transcript expressing cells with activated Kras, inactivated Apc and Trp53 signaling pathways, we crossed Pgc-CreERT2/+ mice with conditional KrasG12D , Apcflox , Trp53 flox mice. Results: Expectedly, mCherry mainly labeled chief cells in the Pgc-CreERT2 mice. However, mCherry was also detected throughout the neck cell and isthmal stem/progenitor regions, albeit at lower levels. In the Pgc-CreERT2;Kras G12D/+ mice, PGC-transcript expressing cells with Kras G12D/+ mutation presented pseudopyloric metaplasia. The early induction of proliferation at the isthmus may reflect the ability of isthmal progenitors to react rapidly to Pgc-driven Kras G12D/+ oncogenic mutation. Furthermore, Pgc-CreERT2;KrasG12D/+ ;Apc flox/flox mice presented intramucosal dysplasia/carcinoma, while Pgc-CreERT2;KrasG12D/+ ;Apcflox/flox ;Trp53 flox/flox mice presented invasive and metastatic gastric carcinoma. Conclusions: The Pgc-CreERT2 knock-in mouse is an invaluable tool to study the effects of successive oncogenic activation in the mouse corpus. Time-course observations can be made regarding the responses of isthmal and chief cells to oncogenic insults. We can observe stomach-specific tumorigenesis from the beginning to metastatic development.

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Distinct immune microenvironments between primary and paired metastatic tumors in gastric cancer patients

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