Macrophage-Tumor Cell Interaction Promotes ATRT Progression and Chemoresistance (GEMM)
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ABSTRACT:
PROVIDER: PRJNA593826 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10597138.fastq.gz | Fastqsanger.gz | |||
| SRR10597139.fastq.gz | Fastqsanger.gz | |||
| SRR10597140.fastq.gz | Fastqsanger.gz | |||
| SRR10597141.fastq.gz | Fastqsanger.gz | |||
| SRR10597142.fastq.gz | Fastqsanger.gz |
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Project description:Macrophage-Tumor Cell Interaction Promotes ATRT Progression and Chemoresistance
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Project description:Atypical teratoid/rhabdoid tumors (ATRT) are known for their heterogeneity concerning pathophysiology and outcome. However, predictive factors within distinct subgroups still need to be uncovered. Using multiplex immunofluorescent staining and singe-cell RNA sequencing we unraveled distinct compositions of the immunological tumor microenvironment (TME) across ATRT subgroups. CD68+ cells predominantly infiltrate ATRT-SHH and ATRT-MYC and are a negative prognostic factor for patients’ survival. Within the murine ATRT-MYC and ATRT-SHH TME, Cd68+ macrophages are core to intercellular communication with tumor cells. In ATRT-MYC distinct tumor cell phenotypes express macrophage marker genes. These cells are involved in the acquisition of chemotherapy resistance in our relapse xenograft mouse model. In conclusion, the tumor cell-macrophage interaction contributes to ATRT-MYC heterogeneity and tumor recurrence.
2020-05-14 | GSE141533 | GEO
Project description:Macrophage-Tumor Cell Interaction Promotes ATRT Progression and Chemoresistance (NODSCID)
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Project description:This SuperSeries is composed of the SubSeries listed below.
2020-05-14 | GSE141534 | GEO
Project description:AMBRA1 interaction mapping in ATRT cellular model to identify potential interaction partners. BT12, BT16, CHLA06 and CHLA266 were used as cellular model. following AP data were analyzed using DIA-NN and interactions were scored against empty FLAG results.
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Project description:Atypical teratoid/rhabdoid tumor (ATRT) is one of the most common brain tumors in infants. Although the prognosis of ATRT patients is poor, some patients respond favorably to current treatments, suggesting molecular inter-tumor heterogeneity. To investigate this further, we genetically and epigenetically analyzed a large series of human ATRTs. Three distinct molecular subgroups of ATRTs, associated with differences in demographics, tumor location, and type of SMARCB1 alterations, were identified. Whole-genome DNA and RNA sequencing found no recurrent mutations in addition to SMARCB1 that would explain the differences between subgroups. Whole-genome bisulfite sequencing and H3K27Ac chromatin-immunoprecipitation sequencing of primary tumors, however, revealed clear differences, leading to the identification of subgroup-specific regulatory networks and potential therapeutic targets. 49 ATRT samples were selected for RNA extraction and hybridization on Affymetrix Affymetrix Human Genome U133 Plus 2.0 Arrays. ---------------------------------------- This submission consists of the expression data for 49 of 170 samples only
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Project description:Background: Cholangiocarcinoma (CCA) is a high malignancy, rapid progression tumor of bile duct. Due to its chemoresistance, it always has an extremely poor prognosis. Therefore, it is still need to detailed elucidation the mechanisms of chemoresistance and find the therapeutic targets. Methods: We analysis the expression of MBD2 in CCA and normal bile duct tissues through public database and immunohistochemical (IHC). The role of MBD2 in CCA cells’ proliferation, migration, chemoresistance ability was validated through CCK-8, plate clone assay, wound healing assay, xenograft mice models. Besides, we construct a primary CCA mice model to further confirm the effect of MBD2. RNA-seq, co-IP-MS were used to find the mechanisms of MBD2 leading to chemoresistance. Results: MBD2 is up-regulated in CCA. It could promote the proliferation, migration and chemoresistance of CCA cells. Mechanistically, MBD2 could directly interact with WDR5, and binding to the promoter of ABCB1, then promote the tri-methylation of H3K4 in this region through KMT2A, active the expression of ABCB1. Knocking down of WDR5 or KMT2A could block the transcriptional activation of ABCB1 by MBD2. MM-102 is a molecular inhibitor that targets the interaction of WDR5 with KMT2A. MM-102 could inhibit the expression of ABCB1 in CCA cells, and decrease the chemoresistance of CCA to cisplatin. Conclusion: MBD2 promote the progress and chemoresistance of CCA through interact with WDR5. MM-102 could effectively block this procedure and enhance the sensitivity to cisplatin of CCA.
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