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Transcriptional heterogeneity of HCC1143 Triple Negative Breast Cancer perturbed with paclitaxel or soluble ligand

ABSTRACT: Transcriptional heterogeneity of HCC1143 Triple Negative Breast Cancer perturbed with paclitaxel or soluble ligand

PROVIDER: PRJNA1108740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR28956577.fastq.gz	Fastqsanger.gz
	SRR28956578.fastq.gz	Fastqsanger.gz
	SRR28956579.fastq.gz	Fastqsanger.gz
	SRR28956580.fastq.gz	Fastqsanger.gz

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Transcriptional heterogeneity of HCC1143 Triple Negative Breast Cancer perturbed with paclitaxel or soluble ligand

Project description:Triple Negative Breast cancer is a heterogeneous disease that is capable of adapting to a variety of stimuli. To study the dynamics of both drug and ligand response, we performed scRNA-seq to deeply profiled the transcriptional response of the HCC1143 cell line to a variety of stimuli.

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Transcriptional effects of soluble CD40 ligand on human naïve B cells

Project description:We performed microarray analysis to derive gene signatures down-stream of soluble CD40 ligand stimulation in human naive B cells. Naïve B cells were purified from healthy donor PBMC using negative selection beads (Miltenyi) and cultured with sCD40L at 2.5ug/ml for 6hr before microarray analysis. In the same study, cells were also harvested at day 5 post-stimulation to confirm sCD40L-induced B cell activation and proliferation. FACS analysis confirmed soluble CD40L induced up-regulation of CD86 and CD69 at 24hr. B cell proliferation was measured at day 4 post-stimulation by EdU incorporation.

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Synthetic lethality of paclitaxel and afatinib in MDA-MB-231 cells

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A chemical screen identifies PRMT5 as a therapeutic vulnerability for paclitaxel-resistant triple-negative breast cancer

Project description:Paclitaxel -resistant triple negative breast cancer (TNBC) remains one of the most challenging breast cancers to treat. Using an epigenetic chemical probe screen, we uncover an acquired vulnerability of paclitaxel-resistant TNBC cells to protein arginine methyltransferases (PRMTs) inhibition. Analysis of cell lines and in-house clinical samples demonstrates that resistant cells evade paclitaxel killing through stabilizing mitotic chromatin assembly. Genetic or pharmacologic inhibition of PRMT5 alters RNA splicing, particularly intron retention of Aurora kinases B (AURKB), leading to a decrease in protein expression, and finally results in selective mitosis catastrophe in paclitaxel-resistant cells. These findings are fully recapitulated in a patient derived xenograft (PDX) model generated from a paclitaxel-resistant TNBC patient, providing the rationale for targeting PRMTs in paclitaxel-resistant TNBC.

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Targeting of apoptotic pathways by SMAC or BH3 mimetics distinctly sensitizes paclitaxel-resistant triple negative breast cancer cells

Project description:Standard chemotherapy is the only systemic treatment for triple-negative breast cancer (TNBC). Despite the good initial responses, resistance remains a major therapeutic obstacle. Here, we employed a High-Throughput Screen to identify targeted therapies that overcome chemoresistance in TNBC. We applied short-term paclitaxel treatment and screened 320 small-molecule inhibitors of known targets to identify drugs that preferentially and efficiently target paclitaxel-treated TNBC cells. Among these compounds the SMAC mimetics (BV6, Birinapant) and BH3-mimetics (ABT-737/263) were recognized as potent targeted therapy for multiple paclitaxel-residual TNBC cell lines. However, acquired paclitaxel resistance through repeated paclitaxel pulses result in desensitization to BV6, but not to ABT-263, suggesting that short- and long-term paclitaxel resistance are mediated by distinct mechanisms. Gene expression profiling of paclitaxel-residual, -resistant and naïve MDA-MB-231 cells demonstrated that paclitaxel-residual, as opposed to -resistant cells, were characterized by an apoptotic signature, with downregulation of anti-apoptotic genes (BCL2, BIRC5), activation of apoptosis inducers (IL24, PDCD4), and enrichment of TNFα/NF-κB pathway, including upregulation of TNFSF15, coupled with cell-cycle arrest. BIRC5 and FOXM1 downregulation and IL24 induction was also evident in breast cancer patient datasets following taxane treatment. Exposure of naïve and paclitaxel-resistant cells to supernatants of paclitaxel-residual cells sensitized them to BV6, and treatment with TNFα enhanced the potency of BV6, suggesting that sensitization to BV6 is mediated, at least partially, by secreted factor(s). Our results suggest that administration of SMAC or BH3 mimetics following short-term paclitaxel treatment could be an effective therapeutic strategy for TNBC, while only BH3-mimetics could effectively overcome long-term paclitaxel resistance

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Project description:Primary outcome(s): Correlation between PD-L1 expression in immune cells and soluble PD-L1 value. Correlation between PD-L1 expression in immune cells or soluble PD-L1 value and PD-L1 expression in tumor tissue. Characterstics of PD-L1 expression in immune cells or soluble PD-L1 value in each gastrointestinal cancer type.

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Project description:Cell cycle inhibitors, including paclitaxel, are among the most widely used and effective cancer therapies. However, several challenges limit the success of paclitaxel including drug resistance and toxic side effects. Paclitaxel is thought to act primarily by stabilizing microtubules and locking cells in a mitotic state. However, the resulting cytotoxicity and tumor shrinkage rates observed cannot be fully explained by this mechanism alone. Here we apply quantitative chemical cross-linking with mass spectrometry analysis to paclitaxel treated cells. Our results provide large scale measurements of relative protein levels and, perhaps more importantly, changes to protein conformations and interactions that occur upon paclitaxel treatment. Drug concentration dependent changes are revealed in known drug targets including tubulins, as well as many other proteins and protein complexes involved in apoptotic signaling and cellular homeostasis. As such this study provides insight into systems-level changes to protein structures and interactions which occur with paclitaxel treatment.

2019-11-21 | PXD015751 | Pride

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Project description:Purpose: Triple Negative Breast Cancer (TNBC) is a particularly aggressive form of breast cancer with high intertumoral and intratumoral heterogeneity. Our overall goal in this study is to investigate the heterogeneity of TNBC, and develop effective combination therapy. Methods: We applied HCC1143 cell line as a representative of aggressive TNBC and performed single cell RNA-seq with 10x genomics platform for cells before and after paclitaxel treatment. Different cell subpopulations were identified with Seurat, and the relationship between different subpoulations were investigated with scEpath. Results: Different subpopulations were detected in TNBC cell populations. Targetable genes were identified and some of them were validated with drug.

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A chemical screen identifies PRMT5 as a therapeutic vulnerability for paclitaxel-resistant triple-negative breast cancer

Project description:Through chemical probe screening, we uncovered a novel mechanism of RNA splicing in paclitaxel-resistant TNBC and identified PRMTs as therapeutic targets.

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A phase Ib trial evaluating the safety, efficacy, and immunologic effects of pembrolizumab plus paclitaxel or flat-dose capecitabine in 1st/2nd line metastatic triple-negative breast cancer

Project description:Chemoimmunotherapy with anti-programmed cell death 1/ligand 1 and cytotoxic chemotherapy is a promising therapeutic modality for women with triple-negative breast cancer, but questions remain regarding optimal chemotherapy backbone and biomarkers for patient selection. We report final outcomes from a phase Ib trial evaluating pembrolizumab (200mg IV every 3 weeks) with either weekly paclitaxel (80mg/m2 weekly) or flat-dose capecitabine (2000mg orally twice daily for 7 days of every 14-day cycle) in the 1st/2nd line setting. The primary endpoint is safety (receipt of 2 cycles without grade III/IV toxicities requiring discontinuation or ≥21-day delays). The secondary endpoint is efficacy (week 12 objective response). Exploratory aims are to characterize immunologic effects of treatment over time, and to evaluate novel biomarkers. The trial demonstrates that both regimens meet the pre-specified safety endpoint (paclitaxel: 87%; capecitabine: 100%). Objective response rate is 29% for pembrolizumab/paclitaxel (n=4/13, 95% CI: 10-61%) and 43% for pembrolizumab/capecitabine (n=6/14, 95% CI: 18-71%). Partial responses are observed in two subjects with chemo-refractory metaplastic carcinoma (both in capecitabine arm). Both regimens are associated with significant peripheral leukocyte contraction over time. Response is associated with clinical PD-L1 score, non-receipt of prior chemotherapy, and the H&E stromal tumor infiltrating lymphocyte score, but also by a novel 27 gene IO score and spatial biomarkers (lymphocyte spatial skewness). In conclusion, pembrolizumab with paclitaxel or capecitabine is safe and clinically active. Both regimens are lymphodepleting, highlighting the competing immunostimulatory versus lymphotoxic effects of cytotoxic chemotherapy. Further exploration of the IO score and spatial TIL biomarkers is warranted.

2023-02-17 | GSE225078 | GEO

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