Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27451169_subreads.fastq.gz | Fastqsanger.gz |
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Project description:Tumor-associated macrophages contribute to tumor pathogenesis and represent an attractive therapeutic target. We report that the proprotein convertase PC1/3 inhibits the TLR4 Myd88-pathway induced in macrophages by the anti-cancer agent Taxol. Thus, PC1/3 knock-down in these cells exacerbates the TLR4 MyD88-dependent pathway triggered by Taxol. In PC1/3 knock-down macrophages, Taxol drives the secretion of pro-inflammatory cytokines, inhibits STAT3 signaling and counteracts tumor-supportive activities, thus inhibiting viability, growth and invasion of glioblastoma cells. Proteomic analyses indicate that their secretomes are characterized by a unique protein profile supporting a specific paracrine anti-tumoral effect. These findings unravel the potential value of a new therapeutic strategy combining PC1/3 inhibition and activation of the TLR4 MyD88-dependent pathway to switch intra-tumoral macrophages toward an anti-tumoral immunophenotype.
2018-03-19 | PXD004444 | Pride
Project description:We identified two effective fungal elicitors, L01 (Guignardia) and J02 (Diaporthe). The two fungal elicitors might activate Taxol biosynthesis by regulating the MYC2a-controlled JA signaling pathway.
2024-04-08 | GSE263216 | GEO
Project description:The purpose of this study is to approach overexpression of TLR4 which contributes the drug resistance in ovarian cancer cells. However, curcumin overcomes this effects. Comparison of the transcriptional regulated genes were performed: (1) analysis of TLR4-overexpressing (T4) and mock (MCS) SKOV3 cells by taxol treatment; (2) assay of taxol alone and combined with curcumin treatments in TLR4-overexpressing (T4) SKOV3 cells. Differential expression analysis was performed with ≥ 2-fold or ≤0.5-fold (p<0.05) changed expression for pathway enrichment analysis.
2022-08-02 | GSE135279 | GEO
Project description:The natural product taxol is an efficient and worldwide accepted anticancer drug. Taxol and other taxoids accumulate in only a few specific genera of the Taxaceae family, such as Taxus and Pseudotaxus. The comprehensive variations among three Taxaceae trees, including one taxol-producing (TP) and two non-taxol producing (NTP) trees, were compared. In total, 3,655 metabolites and 88,609 functional genes were identified through metabolomic and transcriptomic analyses, respectively. KEGG enrichment analysis showed that many differentially expressed genes were enriched in several hormone-, flavonoid-, and terpenoid-related metabolic pathways. The hormones, abscisate and abscisic acid, highly accumulated in the NTP trees, whereas gibberellic acids substantially accumulated in the TP trees.
2018-10-27 | GSE121831 | GEO
Project description:As a sister genus to Taxus, Pseudotaxus holds significant importance for studying the origin and evolution of the taxane biosynthesis pathway. However, the reference genome of P. chienii, the sole species of Pseudotaxus, is not yet available. We have completed a chromosome-level genome assembly of P. chienii, with a total length of 15.6 Gb. P. chienii possesses only a partial pathway for Taxol biosynthesis, which terminates before the enzyme taxane 2α-O-benzoyl transferase (TBT), a crucial enzyme responsible for the production of 10-deacetylbaccatin III. With the emergence of the Taxus genus, the limitation posed by TBT is overcome, allowing for the extension of the existing taxane biosynthesis pathway into a complete Taxol biosynthesis pathway. Protein structure analysis revealed that the structure of metal ion catalysis sites in taxadiene synthase (TS) is conserved across the Pseudotaxus and Taxus genera, providing potential sites for enhancing TS activity through enzyme engineering. This comparative genomic analysis contributes to our understanding of the origin and evolution of taxane biosynthesis within the Taxaceae family.
2025-01-27 | GSE288094 | GEO
Project description:Triple-negative breast cancer (TNBC) stands out as a particularly aggressive and frequently recurring form of breast cancer. Due to the absence of hormone receptors, the available treatment avenues are constrained, making chemotherapy the primary approach. Unfortunately, the development of resistance to chemotherapy poses a significant challenge, further restricting the already limited therapeutic alternatives for recurrent cases. Understanding the molecular basis of chemotherapy resistance in TNBC is pivotal for improving treatment outcomes. Here, we generated two different Taxol-resistant TNBC cell lines with dose-escalation method to mimic chemotherapy resistance in vitro. These cells exhibited hallmark features of resistance, including reduced cell growth, altered morphology, and resistance to apoptosis. Transcriptome analysis uncovered elevated ABCB1 expression and multidrug-resistant phenotype in the resistant cells. To comprehensively investigate the key epigenetic regulators of Taxol resistance, we conducted epigenome-wide CRISPR/Cas9 and chemical probe library screens. Both screens pinpointed Bromodomain and PHD Finger Containing 1 (BRPF1) which is the reader protein in MOZ/MORF histone acetyl-transferase complex, as the regulator of Taxol resistance in TNBC cells. Knockout of BRPF1, but not the other members of the MOZ/MORF complex, sensitized resistant cells to Taxol. Additionally, BRPF1 inhibitors, PFI-4 and OF-1, in combination with Taxol significantly reduced cell viability. Transcriptome analysis upon BRPF1 loss or inhibition revealed a negative impact on ribosome biogenesis-related gene sets, resulting in a global decrease in protein translation in Taxol-resistant cells. Our ChIP-qPCR analysis further demonstrated that active BRPF1 directly interacts with the ABCB1 promoter, enhancing its expression and inducing a multidrug-resistant phenotype. Conversely, knockout or inhibition of BRPF1 leads to decreased ABCB1 expression. This dual mechanism critically sensitizes Taxol-resistant TNBC cells to chemotherapy. Our findings uncover a comprehensive molecular framework, highlighting the pivotal role of epigenetic reader protein BRPF1 in Taxol resistance and providing potential avenues for therapeutic intervention in TNBC.
2024-05-14 | GSE262353 | GEO
Project description:Triple-negative breast cancer (TNBC) stands out as a particularly aggressive and frequently recurring form of breast cancer. Due to the absence of hormone receptors, the available treatment avenues are constrained, making chemotherapy the primary approach. Unfortunately, the development of resistance to chemotherapy poses a significant challenge, further restricting the already limited therapeutic alternatives for recurrent cases. Understanding the molecular basis of chemotherapy resistance in TNBC is pivotal for improving treatment outcomes. Here, we generated two different Taxol-resistant TNBC cell lines with dose-escalation method to mimic chemotherapy resistance in vitro. These cells exhibited hallmark features of resistance, including reduced cell growth, altered morphology, and resistance to apoptosis. Transcriptome analysis uncovered elevated ABCB1 expression and multidrug-resistant phenotype in the resistant cells. To comprehensively investigate the key epigenetic regulators of Taxol resistance, we conducted epigenome-wide CRISPR/Cas9 and chemical probe library screens. Both screens pinpointed Bromodomain and PHD Finger Containing 1 (BRPF1) which is the reader protein in MOZ/MORF histone acetyl-transferase complex, as the regulator of Taxol resistance in TNBC cells. Knockout of BRPF1, but not the other members of the MOZ/MORF complex, sensitized resistant cells to Taxol. Additionally, BRPF1 inhibitors, PFI-4 and OF-1, in combination with Taxol significantly reduced cell viability. Transcriptome analysis upon BRPF1 loss or inhibition revealed a negative impact on ribosome biogenesis-related gene sets, resulting in a global decrease in protein translation in Taxol-resistant cells. Our ChIP-qPCR analysis further demonstrated that active BRPF1 directly interacts with the ABCB1 promoter, enhancing its expression and inducing a multidrug-resistant phenotype. Conversely, knockout or inhibition of BRPF1 leads to decreased ABCB1 expression. This dual mechanism critically sensitizes Taxol-resistant TNBC cells to chemotherapy. Our findings uncover a comprehensive molecular framework, highlighting the pivotal role of epigenetic reader protein BRPF1 in Taxol resistance and providing potential avenues for therapeutic intervention in TNBC.
2024-05-14 | GSE262577 | GEO
Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578T) upon treatment with UNC1999 3uM Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)
2020-08-18 | GSE111920 | GEO
Project description:Taxol is an efficient anticancer drug accumulated in Taxus trees. Taxus media, a large-scale cultured species, is a dioecious woody tree with high taxol yielding. However, the sexually dimorphic accumulation of taxoids in T. media is largely unknown. Our study identified a large number of differentially accumulated metabolites and differentially expressed genes, revealing the comprehensive differences between the female and male T. media trees. LC-MS analysis confirmed the high accumulation of taxoids in the female trees. Expression analysis showed that most Taxol biosynthesis-related genes were predominantly expressed in the female trees. To investigate the regulation mechanism underlying the sexually dimorphic accumulation of taxoids, a female-specific expressed gene, TmMYB39, was identified and its full-length sequence was cloned. Multiple sequence alignment and phylogenetic analyses showed that TmMYB39 is a typical R2R3-MYB factor and the subcellular localization of TmMYB39 is shown to be the nucleus. Furthermore, Y2H and BiFC assays showed that TmMYB39 interacts with TmbHLH13. Partial promoter sequences of 10 taxol biosynthesis-related genes were isolated, which were used for screening of the MYB recognition elements. TmMYB39 binds to the promoters of several taxol-related genes, such as GGPPS, T7OH, T10OH, T13OH, and TBT genes. Interaction between TmMYB39 and TmbHLH13 affected the expression of GGPS and T10OH genes, suggesting that TmMYB39 might function in the regulation of taxol biosynthesis through a ‘MYB-bHLH’ module. Our data provided a potential explanation for the sexually dimorphic accumulation of taxoids.
2021-05-28 | GSE175645 | GEO
Project description:Mouse lymphoma L5178Y cells are treated with Taxol (Paclitaxel) [CAS:33069-62-4;CHEBI:7887] and harvested at 4 and 24 hours for analysis.
2004-02-13 | E-TOXM-9 | biostudies-arrayexpress