Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13526300_1.fastq.gz | Fastqsanger.gz | |||
| SRR13526300_2.fastq.gz | Fastqsanger.gz | |||
| SRR13526400.fastq.gz | Fastqsanger.gz | |||
| SRR13526301_1.fastq.gz | Fastqsanger.gz | |||
| SRR13526301_2.fastq.gz | Fastqsanger.gz |
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Project description:DNA methylation data of PAC PDX models before Gemcitabine treatment
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Project description:DNA methylation data of PAC PDX models after Gemcitabine treatment
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Project description:We report that eight gene products were downregulated in PA4 and PA16 PDX models by BET inhibitor JQ1 + gemcitabine, compared to vehicle controls.
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Project description:Endocrine therapies (ET) combined with CDK4/6 inhibition (CDK4/6i) is standard treatment for estrogen receptor-α-positive (ER+) breast cancer, however lethal drug resistance is common. Proteogenomic analyses of 22 ER+ breast cancer patient-derived xenografts (PDXs) demonstrated that PKMYT1, a WEE1 homolog, is highly estradiol (E2) regulated in E2-dependent PDXs and constitutively expressed when growth is E2 independent. In clinical samples, high PKMYT1 mRNA is a resistance biomarker for both ET and CDK4/6 inhibition. The PKMYT1 inhibitor lunresertib(RP-6306) and gemcitabine selectively and synergistically reduced the viability of ET and palbociclib-resistant ER+ breast cancer cells without functional p53 in vitro; the combination increased DNA damage and apoptosis. In palbociclib-resistant, TP53 mutant PDX organoids and xenografts, RP-6306 with low-dose gemcitabine induced greater tumor volume reduction compared to treatment with either single agent. These results demonstrate the clinical potential of RP-6306 in combination with gemcitabine for ET and CDK4/6i resistant TP53 mutant ER+ breast cancer.
2025-05-13 | PXD050619 | Pride
Project description:Tumor-stroma interactions are critical in pancreatic ductal adenocarcinoma (PDAC) progression and therapeutics. Patient-derived xenograft (PDX) models faithfully recapitulate tumor-stroma interactions in PDAC, but conventional antibody-based immunoassay is largely inadequate to resolve or quantify tumor and stromal proteins. A species-deconvolved proteomics approach embedded in the ultra-high-resolution (UHR)-IonStar workflow can unambiguously quantify the proteins from tumor (human-derived) and stroma (mouse-derived) in PDX samples, enabling unbiased investigation of their proteomes with excellent quantitative reproducibility. With this strategy, 3 PDAC PDXs were analyzed. They were showed differential responses to treatment with Gemcitabine combined with nab-Paclitaxel (GEM+PTX), which is a first-line treatment regimen for PDAC. For each PDAC PDX, samples were collected after 24 hour and 192 hour with/without treatment, and each condition contained four biological replicates.
2023-07-05 | PXD042267 | Pride
Project description:Aims: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with poor prognosis, and gemcitabine-based chemotherapy remains the standard first-line treatment. However, the rapid emergence of chemoresistance limits its efficacy. Elucidating the molecular mechanisms underlying gemcitabine resistance is critical for improving therapeutic outcomes. Approaches & Results: By integrating transcriptomic profiling of gemcitabine-resistant PDAC cells, patient-derived xenografts (PDXs), and pretreatment clinical biopsy specimens, we identified the m6A reader IGF2BP1 as a key determinant of both intrinsic and acquired gemcitabine resistance. Mechanistically, IGF2BP1 directly binds m6A-modified FTH1 mRNA and cooperates with G3BP1-mediated stress granule sequestration to enhance FTH1 transcript stability under chemotherapeutic stress. The stabilized FTH1 maintains intracellular iron homeostasis, limits lipid peroxidation, and suppresses ferroptosis, thereby conferring chemoresistance. Pharmacological inhibition of IGF2BP1 with BTYNB partially disrupted this regulatory axis, restored ferroptotic susceptibility, and synergistically enhanced gemcitabine efficacy in resistant PDX models without overt toxicity. Conclusions: Collectively, this study uncovers a previously unrecognized epitranscriptomic mechanism linking m6A-dependent RNA stabilization, stress granule dynamics, and ferroptosis suppression in PDAC. By identifying IGF2BP1 as a potential biomarker of gemcitabine response and a therapeutically actionable target, these findings provide a preclinical rationale for IGF2BP1-targeted combination strategies to overcome gemcitabine resistance in PDAC.
2026-08-19 | GSE337104 | GEO
Project description:Aims: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with poor prognosis, and gemcitabine-based chemotherapy remains the standard first-line treatment. However, the rapid emergence of chemoresistance limits its efficacy. Elucidating the molecular mechanisms underlying gemcitabine resistance is critical for improving therapeutic outcomes. Approaches & Results: By integrating transcriptomic profiling of gemcitabine-resistant PDAC cells, patient-derived xenografts (PDXs), and pretreatment clinical biopsy specimens, we identified the m6A reader IGF2BP1 as a key determinant of both intrinsic and acquired gemcitabine resistance. Mechanistically, IGF2BP1 directly binds m6A-modified FTH1 mRNA and cooperates with G3BP1-mediated stress granule sequestration to enhance FTH1 transcript stability under chemotherapeutic stress. The stabilized FTH1 maintains intracellular iron homeostasis, limits lipid peroxidation, and suppresses ferroptosis, thereby conferring chemoresistance. Pharmacological inhibition of IGF2BP1 with BTYNB partially disrupted this regulatory axis, restored ferroptotic susceptibility, and synergistically enhanced gemcitabine efficacy in resistant PDX models without overt toxicity. Conclusions: Collectively, this study uncovers a previously unrecognized epitranscriptomic mechanism linking m6A-dependent RNA stabilization, stress granule dynamics, and ferroptosis suppression in PDAC. By identifying IGF2BP1 as a potential biomarker of gemcitabine response and a therapeutically actionable target, these findings provide a preclinical rationale for IGF2BP1-targeted combination strategies to overcome gemcitabine resistance in PDAC.
2026-08-19 | GSE337103 | GEO
Project description:Aims: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with poor prognosis, and gemcitabine-based chemotherapy remains the standard first-line treatment. However, the rapid emergence of chemoresistance limits its efficacy. Elucidating the molecular mechanisms underlying gemcitabine resistance is critical for improving therapeutic outcomes. Approaches & Results: By integrating transcriptomic profiling of gemcitabine-resistant PDAC cells, patient-derived xenografts (PDXs), and pretreatment clinical biopsy specimens, we identified the m6A reader IGF2BP1 as a key determinant of both intrinsic and acquired gemcitabine resistance. Mechanistically, IGF2BP1 directly binds m6A-modified FTH1 mRNA and cooperates with G3BP1-mediated stress granule sequestration to enhance FTH1 transcript stability under chemotherapeutic stress. The stabilized FTH1 maintains intracellular iron homeostasis, limits lipid peroxidation, and suppresses ferroptosis, thereby conferring chemoresistance. Pharmacological inhibition of IGF2BP1 with BTYNB partially disrupted this regulatory axis, restored ferroptotic susceptibility, and synergistically enhanced gemcitabine efficacy in resistant PDX models without overt toxicity. Conclusions: Collectively, this study uncovers a previously unrecognized epitranscriptomic mechanism linking m6A-dependent RNA stabilization, stress granule dynamics, and ferroptosis suppression in PDAC. By identifying IGF2BP1 as a potential biomarker of gemcitabine response and a therapeutically actionable target, these findings provide a preclinical rationale for IGF2BP1-targeted combination strategies to overcome gemcitabine resistance in PDAC.
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Project description:The molecular basis underlying the known anti-inflammatory and anticarcinogenic properties of cranberries is incompletely understood. We investigated the microRNA (miRNA)-modulatory effects of cranberry proanthocyanidin (PAC) and two of its main gut microbial metabolites, 3,4-dihydroxyphenylacetic acid (DHPAA) and 3-(4-hydroxyphenyl)-propionic acid (HPPA), in intestinal cells at homeostasis and in inflammatory conditions. Differentiated Caco-2BBe1 cells were pre-treated with PAC, DHPAA, or HPPA then stimulated with IL-1ß or not. Total RNA was used to profile the expression of 799 miRNAs. PAC, DHPAA, and HPPA generated subsets of shared and distinct miRNA responses. At homeostasis, miRNAs affected by the metabolites, but not by PAC, targeted genes enriched in kinase, Wnt, and growth factor signaling, cell growth and proliferation, apoptosis, and specific cancer pathways. In an inflammatory environment, pre-treatment with PAC and DHPAA, but not HPPA, reversed the expression of 16 and two IL-1ß-induced miRNAs, targeting genes enriched in inflammatory and cancer pathways. These data suggest that in the absence of inflammation, PAC may be reliant on its transformation by the gut microbiota for its miRNA-modulatory effects, while in an inflammatory environment, both PAC and DHPAA counter inflammatory miRNA responses. This work provides a novel mechanism to characterize the bioactivity of cranberry and will inform cranberry utilization in nutritional strategies for the maintenance of intestinal homeostasis.
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