RNA-Seq analysis identifies to GATA3-AS1 as a lncRNA associated with resistance to neoadjuvant chemotherapy in locally advanced breast cancer patients
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ABSTRACT:
PROVIDER: PRJNA668985 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12817525_1.fastq.gz | Fastqsanger.gz | |||
| SRR12817525_2.fastq.gz | Fastqsanger.gz | |||
| SRR12817526_1.fastq.gz | Fastqsanger.gz | |||
| SRR12817526_2.fastq.gz | Fastqsanger.gz | |||
| SRR12817527_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Identified the expression profile of lncRNA associated to neoadjuvant chemotherapy response in 11 tumor of locally advanced breast cancer patients Methods: We implemented the transcriptomic analysis from 11 breast cancer samples by paired-end RNA-Seq, as a case-control study (responders vs nonresponders group). Differential expression analysis for lncRNA and mRNA were made to identify lncRNA as predictive biomarkers. Results: We identified the over-expressed lncRNA GATA3-AS1 in nonresponders group. Additionally, we identified the pathways were differentially expressed lncRNA and mRNA are associated in neoadjuvant chemotherapy response. Conclusion: we propose lncRNA GATA3-AS1 as a potential predictive biomarker for patients with LABC luminal B-like subtype that will not respond to neoadjuvant chemotherapy
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Project description:Purpose: Identified the expression profile of lncRNAs associated to neoadjuvant chemotherapy response in 47 luminal B tumors of locally advanced breast cancer patients Methods: We implemented the transcriptomic analysis from 47 luminal B breast cancer samples by paired-end RNA-Seq, as a case-control study (responders vs nonresponders group). Differential expression analysis for lncRNA and mRNA were made to identify lncRNA as predictive biomarkers. Results: We identified a signature of lncRNAs associated with nonresponders group. Additionally, we identified the pathways were differentially expressed lncRNA and mRNA are associated in neoadjuvant chemotherapy response. Additionally, we proposed the clinical application of lncRNA GATA3-AS1 as a predictive biomarker to neoadjuvant chemotherapy response in luminal B breast cancer patients detected by RNA-ISH. Conclusion: we propose the clinical utility of lncRNA GATA3-AS1 detected by RNA-ISH to identify luminal B breast cancer patients that will not respond to neoadjuvant chemotherapy.
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Project description:Background. There is evidence that the stromal compartment may influence breast cancer responsiveness to chemotherapy. Our aim was to detect a stromal cell signature (using a direct approach of microdissected stromal cells) associated with response to neoadjuvant chemotherapy in locally advanced breast cancer, considering tumor down staging (to at least ypT1a/b,ypN0), as the best response. Patients and methods. Forty four patients diagnosed with locally advanced breast cancer (29 classified as estrogen receptor (ER) positive and 15, as ER negative) were included. Neoadjuvant chemotherapy consisted of doxorubicin/cyclophosphamide, followed by paclitaxel. Response was defined as downstaging to maximum ypT1a-b/ypN0. Stromal cells were microdissected from fresh frozen tumor samples and gene expression profile was determined using Agilent SurePrint G3 Human Gene Expression Microarrays. Expression levels were compared using MeV (MultiExperiment Viewer) software, applying SAM (Significance analysis of microarrays). Gene set enrichment analysis was used to identify gene sets correlated with the phenotype downstaging. Results: After chemotherapy, nine patients presented disease downstaging to maximum ypT1a-b/ypN0. Using SAM test (FDR 17), 11 sequences were differentially expressed, all of which (except for H2AFJ) more expressed in responsive tumors. Gene list enrichment analysis revealed three genes involved in abnormal cytotoxic T cell physiology: TOX, LY75 and SH2D1A. Gene sets correlated with tumor downstaging (FDR < 0.01), were mainly involved in immune response or lymphocyte activation, both in ER positive and ER negative samples. Conclusion: In locally advanced breast cancer, stromal cells may present specific features of immune response that may be associated with chemotherapy response.
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Project description:To elucidate candidate genes and pathways associated with poor response, we retrospectively analyzed gene expression profiles in serial biopsies from women with locally advanced breast cancer who failed to respond to anthracycline-based chemo followed by taxane in the I-SPY Of the 221 patients who completed neoadjuvant chemotherapy, 215 patients had surgery with 73% not achieving a pathologic complete response (pathCR). In these patients, cDNA microarray expression profiles from pretreatment biopsy (T1) were compared to those biopsy specimens obtained 24-72 hours after initiation of treatment (T2) or in tumors surgically removed after chemotherapy (TS). Paired expression data for T1vsT2 and T1vsTS were available for 29 and 39 patients with no pathCR, respectively. Paired differential expression analyses were performed via Significance Analysis of Microarrays (SAM) and differentially expressed genes were subjected to Ingenuity Pathway Analysis
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Project description:Host defense against diverse pathogens involves the recruitment and differentiation of CD4+ T effector subsets including T helper 1 (Th1), Th2, Th17 and induced regulatory T (Treg) cells. Surface phenotype studies have revealed subset-specific surface markers for the identification and purification of human primary CD4+ T effector subsets. In the present study, we aimed to characterize the mRNA and large intergenic non-coding RNA (lincRNA) expression differences between human primary CD4+ T effector subsets and identify potential subset-specific genes. To achieve this goal, mRNA and lincRNA microarray profiling of flow cytometry-sorted human primary Th1, Th2, Th17 and Treg cells was performed. Principal component and pathway analyses revealed subset-specific gene expression patterns. A Th2-specific lincRNA, GATA3-AS1, also termed FLJ45983, was identified in primary immune cells and tissues, as well as in in vitro polarized CD4+ T effector subsets. Further analysis showed that GATA3-AS1 was a potential diagnostic marker in allergy, a Th2-associated disease. This first systematic genome-wide analysis of gene expression differences between primary CD4+ T effector subsets may help to identify novel regulatory protein-coding genes and lincRNAs regulating CD4+ T cell subset differentiation, as well as potential diagnostic markers. As an example, we identified a GATA3-associated Th2-specific marker lincRNA GATA3-AS1. Gene expression microarray analysis of flow-cytometry sorted human primary naïve CD4+ T cells, CD4+ T central memory cells, Th1, Th2, Th17 and Treg cells from buffy coat of four healthy controls Gene expression microarray analysis was performed using SurePrint G3 Human Gene Expression 8X60K microarray.
2013-06-01 | E-GEOD-43005 | biostudies-arrayexpress
Project description:Resistance to neoadjuvant chemotherapy is associated tumor recurrence of locally advanced rectal cancer (LARC), which remains an unmet demand to exploit potential therapeutic strategies to improve clinical outcomes. Here we demonstrated that aberrant activation of cell cycle pathways is correlated with resistance to neoadjuvant chemotherapy in LARC. A combinatorial drug screening of 130 kinase inhibitors targeting cell cycle regulators with oxaliplatin identified that CDK4/6 inhibitors synergistically enhanced anti-tumor effects of oxaliplatin both intrinsic and acquired chemo-resistant colon cancer cells. Functional studies in both in vitro and in vivo models showed that CDK4/6 inhibitors significantly increased sensitivity to oxaliplatin. Integrative transcriptomic and chromatin profiling analysis revealed that CDK4/6 inhibitors induced DNA repair defects to enhance sensitivity of oxaliplatin through epigenetically suppression of DNA repair related genes. Mechanistically, CDK4/6 inhibition impairs DNA damage repair through a previously unrecognized RB1/TEAD4/HDAC1 co-repressor complex which contributes to the resistance to neoadjuvant chemotherapy in LARC. Together, our work revealed an important role of CDK4/6 pathway in LARC patients with neoadjuvant chemotherapy, suggesting that targeting CDK4/6 could provide a potentially effective treatment strategy for LARC.
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Project description:Stromal cell signature associated with response to neoadjuvant chemotherapy in locally advanced breast cancer
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Project description:Neoadjuvant chemoradiation therapy (CRT) is a widely used preoperative treatment strategy for locally advanced rectal cancer (LARC). However, a few studies have evaluated the molecular changes caused by neoadjuvant CRT in these cancer tissues. Here, we aimed to investigate changes in immunotherapy-related immunogenic effects in response to preoperative CRT in LARC. We analyzed 60 pairs of human LARC tissues before and after irradiation from three independent LARC cohorts, including a LARC patient RNA sequencing (RNA-seq) dataset from our cohort and GSE15781 and GSE94104 datasets. Gene ontology analysis showed that preoperative CRT significantly enriched the immune response in LARC tissues. Moreover, gene set enrichment analysis revealed six significantly enriched Kyoto Encyclopedia of Genes and Genomes pathways associated with downregulated genes, including mismatch repair (MMR) genes, in LARC tissues after CRT in all three cohorts. Radiation also induced apoptosis and downregulated various MMR system-related genes in three colorectal cancer cells. One patient with LARC showed a change in microsatellite instability (MSI) status after CRT, as demonstrated by the loss of MMR protein and PCR for MSI. Moreover, CRT significantly increased tumor mutational burden in LARC tissues. CIBERSORT analysis revealed that the proportions of M2 macrophages and CD8 T cells were significantly increased after CRT in both the RNA-seq dataset and GSE94104. Notably, preoperative CRT increased various immune biomarker scores, such as the interferon-γ signature, the cytolytic activity and the immune signature. Taken together, our findings demonstrated that neoadjuvant CRT modulated the immune-related characteristics of LARC, suggesting that neoadjuvant CRT may enhance the responsiveness of LARC to immunotherapy.
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