Ontology highlight
ABSTRACT:
PROVIDER: PRJNA994866 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25278406_1.fastq.gz | Fastqsanger.gz | |||
| SRR25278406_2.fastq.gz | Fastqsanger.gz | |||
| SRR25278407_1.fastq.gz | Fastqsanger.gz | |||
| SRR25278407_2.fastq.gz | Fastqsanger.gz | |||
| SRR25278408_1.fastq.gz | Fastqsanger.gz |
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Project description:This project aimed to identify a specific target for chromosome 8p deletions. Using large-scale functional-genomic screening data of over 527 well-characterized cancer cell lines. We were able to identify the dependency of SLC25A28 (Mitoferrin-2, MFRN2), a mitochondrial iron transporter, in chromosome 8p deleted cancer cell lines. Interestingly, we found that SLC25A37 (Mitoferrin-1, MFRN1), the paralog of MFRN2, resides on chromosome 8p and is frequently deleted in liver cancer. We found a strong correlation between the cellular dependency on MFRN2 and the MFRN1 expression levels, possibly explaining why MFRN2 is a synthetic lethal target for 8p deletions. Our study discovered MFRN2 as a target for a therapeutic strategy in chromosome 8p deleted cancer specimens. Further, it revealed MFRN1 as a biomarker that predicts the response to MFRN2-directed therapy.
2024-06-03 | PXD044780 | Pride
Project description:Chromosome arm deletions are frequently observed in human cancers. Such large-scale aberrations may trigger phenotypes distinct from those that arise by loss of single genes. Using TALEN-based genomic engineering, we generated cell models with targeted 8p loss-of-heterozygosity (LOH) that mimics an 8p deletion commonly found in breast cancer patients. 8p LOH triggered up-regulation of the mevalonate pathway. The alterations in lipid metabolism led to increased metastatic potential and drug resistance of 8p-deleted cells that are in agreement with poorer survival rates of breast cancer patients harbouting 8p LOH. Our findings also suggest novel therapeutic strategies for treatment of 8p LOH tumors.
2015-05-21 | GSE68042 | GEO
Project description:Chromosome arm deletions are frequently observed in human cancers. Such large-scale aberrations may trigger phenotypes distinct from those that arise by loss of single genes. Using TALEN-based genomic engineering, we generated cell models with targeted 8p loss-of-heterozygosity (LOH) that mimics an 8p deletion commonly found in breast cancer patients. 8p LOH triggered up-regulation of the mevalonate pathway. The alterations in lipid metabolism led to increased metastatic potential and drug resistance of 8p-deleted cells that are in agreement with poorer survival rates of breast cancer patients harbouting 8p LOH. Our findings also suggest novel therapeutic strategies for treatment of 8p LOH tumors. RNASeq Analysis of two Wt 8p Cell clones vs two 8p LOH cell clones generated via TALEN Approach
2015-05-21 | E-GEOD-68042 | biostudies-arrayexpress
Project description:A large panel of 81 liver cancer cell models, designated as LIver cancer MOdel REpository (LIMORE) was constructed. These cell lines include 31 public cell lines and 50 new cell models establishend from Chinese liver cancer patients. Whole genome sequencing (WGS), exome sequencing (WES) and RNA sequencing (RNAseq) were performed to obtain the genetic information for these cell lines. These cell lines and associated data provide new models and also a rich resource for liver cancer.
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Project description:8p Loss of Heterozygosity triggers metastasis and drug resistance
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Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations. Keywords: Chromosome copy number and LOH analysis with SNP Genotyping Arrays
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Project description:Aneuploidy is prevalent in cancer, conferring fitness advantage, multidrug resistance, and poor prognosis. In contrast, experimentally induced aneuploidy often results in adverse effects and impaired proliferation. This paradox underscores the necessity of cancer cells to adapt to abnormal chromosome numbers. To identify molecular mechanisms of adaptation to aneuploidy, we initiated in vitro evolution of cells with extra chromosomes added via microcell-mediated chromosome transfer. To this end, we cultured cells in a nutrient-rich medium for 50 passages or plated the cells at a low density and selectively collected the largest colonies originating from a single cell (colony selection). One of the striking observations following evolution of cells with extra chromosome 5 in HCT116 cell line was the frequent loss of the 5q, while maintaining the 5p arm after in vitro evolution. Chromosome 5 is a frequent target of large copy number alterations in several malignancies, such as ovarian, gastric, and oesophageal cancer, and malignant myeloid diseases. Moreover, analysis of chromosome arm level events in the TCGA dataset clearly shows that loss of chromosome arm 5q and gain of 5p are among the most frequent events. We asked whether these specific changes in copy numbers of chromosome 5 – loss of 5q with simultaneous retention of 5p – could affect the proliferation of the evolved cells. To this end, we used the recently developed technique ReDACT-TR (Restoring Disomy in Aneuploid cells using CRISPR Targeting with Telomere Replacement (Girish et al., 2023)), and transfected cells of a separate clone of Htr5 (before evolution) with a gRNA that cuts near the centromere of chromosome 5, simultaneously with a cassette encoding ~100 repeats of the human telomere seed sequence. Targeting the q-arm generated two independent cell lines with 5p trisomy (Htr5p_1 and Htr5p_2), which were confirmed by FISH with probes specific for 5p and 5q arms and by shallow WGS. No cell lines with trisomy of the q-arm were generated, but we have obtained two diploid cell lines (Hdi5_1 and Hdi5_2), most likely due to the CRISPR/Cas9 induced loss of chromosome 5 (Papathanasiou, Markoulaki et al., 2021, Tsuchida, Brandes et al., 2023). The anaylsis of global proteomes of the ReDACT cell lines was then carried out using a TMT quantification strategy.
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2008-11-01 | GSE11447 | GEO
Project description:Renal tumors with complex morphology require extensive workup for accurate classification. Chromosomal aberrations that define subtypes of renal epithelial neoplasms have been reported. We explored if whole-genome chromosome copy number and loss-of-heterozygosity analysis with single nucleotide polymorphism (SNP) arrays can be used to identify these aberrations. Experiment Overall Design: We analyzed 20 paraffin-embedded tissues representing conventional renal cell carcinoma (RCC), papillary RCC, chromophobe RCC, and oncocytoma with Affymetrix GeneChip 10K 2.0 Mapping arrays.
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