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Mechanism of enhancing chemotherapy efficacy in pancreatic ductal adenocarcinoma with paricalcitol and hydroxychloroquine

ABSTRACT: Mechanism of enhancing chemotherapy efficacy in pancreatic ductal adenocarcinoma with paricalcitol and hydroxychloroquine

PROVIDER: PRJNA1184174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31299365_1.fastq.gz	Fastqsanger.gz
	SRR31299365_2.fastq.gz	Fastqsanger.gz
	SRR31299366_1.fastq.gz	Fastqsanger.gz
	SRR31299366_2.fastq.gz	Fastqsanger.gz
	SRR31299367_1.fastq.gz	Fastqsanger.gz

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Mechanism of enhancing chemotherapy efficacy in pancreatic ductal adenocarcinoma with paricalcitol and hydroxychloroquine

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a minimal (<15%) five-year existence, in part due to resistance to chemoradiotherapy. Previous research reveals the impact of paricalcitol (P) and hydroxychloroquine (H) on altering the lysosomal fusion, decreasing stromal burden, and triggering PDAC to chemotherapies. This investigation aims to elucidate the molecular properties of the H and P combination and its potential in sensitizing PDAC to gemcitabine (G). PH potentiates the effects of G in in vitro, orthotopic mouse models, and a patient-derived xenograft model of PDAC. Proteomic and single-cell RNAseq analyses reveal that GPH treatment upregulates autophagy and ER stress-related transcripts. GPH treatment decreases the number of Ki67, FAP, and alpha-SMA-expressing fibroblasts with a decrease in autophagy-related transcripts. The GPH treatment increases M1 polarization, CD4+, and CD8+ T-cells and reduces the CD4+ and CD8+ Tregs. These effects of GPH were confirmed in paired biopsies obtained from patients treated in a clinical trial (NCT04524702).

2024-11-09 | GSE281518 | GEO

Paricalcitol and hydroxychloroquine modulates extracellular matrix and enhance chemotherapy efficacy in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with poor prognosis and limited therapeutic options. In a previous publication, our group defined some of the mechanisms that vitamin D analogue paricalcitol (P) and hydroxychloroquine (H) potentiated the effects of gemcitabine-based chemotherapy in PDAC. Based on this, we hypothesized that the mechanisms of potentiation of 5-Fluorouracil (5FU) and oxaliplatin-based chemotherapy by PH may include different pathways than what was seen with gemcitabine-based therapy. Using MIA PaCa-2, HPAC and KPC cell lines, the combination of PH significantly increased the cell death, apoptosis, and S-phase cell cycle arrest. In vivo, the combination therapy inhibited PDAC growth and altered the immune landscape by activating T and NK cells. Proteomic analysis revealed that, significant reduction in ECM proteins, specifically integrin beta-4 (ITGB4) which was also seen with gemcitabine. Furthermore, genetic knockdown of ITGB4 suggested that the ECM inhibiti

2024-11-23 | PXD058209 |

Mechanism of enhancing chemotherapy efficacy in pancreatic ductal adenocarcinoma with paricalcitol and hydroxychloroquine

Project description:Proteomic and single-cell RNAseq analyses reveal that GPH treatment upregulates autophagy and ER stress-related transcripts.

2024-11-20 | PXD058067 |

Increased glucose availability sensitizes pancreatic cancer to chemotherapy

Project description:Pancreatic cancer (Pancreatic Ductal Adenocarcinoma; PDAC) is highly resistant to chemotherapy. Effective alternative therapies have yet to emerge, and therefore, chemotherapy remains the best available systematic treatment. The discovery of safe and available adjuncts that can improve chemotherapeutic efficacy could potentially improve survival outcomes. We show that a hyperglycemic state enhances the efficacy of conventional single- and multi-agent chemotherapies against PDAC. Molecular analyses of tumors exposed to relatively high glucose levels revealed that GCLC (catalytic subunit of glutamate-cysteine ligase), a key regulator of a metabolic pathway, glutathione biosynthesis, is diminished and underlies chemo-sensitization. Inhibition to GCLC phenocopied the effect of an induced hyperglycemic state in mouse models of PDAC, while rescuing the pathway abrogated the anti-tumor effects observed with chemotherapy treatment under high glucose conditions.

2022-10-18 | MTBLS6000 | MetaboLights

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Hydroxychloroquine inhibits trained immunity

Project description:We demonstrate that hydroxychloroquine inhibits trained immunity at the functional and epigenetic level and is accompanied by reduced expression of interferon-stimulated genes. Trained immunity comprises a functional adaptation induced by epigenetic reprogramming which facilitates the anti-viral innate immune response.

2020-10-21 | GSE159678 | GEO

Gene expression-profiling to predict induction chemotherapy efficacy in locoregionally advanced nasopharyngeal carcinoma

Project description:Gene expression signature can be used to predict treatment efficacy in various types of tumour. We aim to identify a gene expression signature to predict efficacy of induction chemotherapy (IC) in patients with locoregionally advanced nasopharyngeal carcinoma (LA-NPC).

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Microbiota-derived 3-IAA influences chemotherapy efficacy in pancreatic cancer

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Riluzole Enhancing anti-PD-1 Efficacy by Activating cGAS/STING Signaling

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RNA-seq of THP-1 cells stimulated with CpG-c and Hydroxychloroquine intervention

Project description:Purpose: To investigate the inhibition of inflammatoty cytokines of Hydroxychloroquine to phagocytic THP-1 cells. Methods: we established a cell model of hemophagocytosis by simulating THP-1 cells with CpG-c for 24h in vitro to produce macrophages, and then coculture the cells with human RBCs. RNA sequencing analysis of THP-1 cells were performed to find Gene changed with CpG-c stimulation and Hydroxychloroquine intervention. Results:CpG-c sitimulation significantly altered gene expression of THP-1 cells. Cytokine genes were upregulated, especially a significant increase in IL-6 level from scratch. HCQ significantly inhibited the expression of inflammatory cytokines and decreased IL-6 gene level to baseline. Conclusions:Hydroxychloroquine can inhibite cytokine genes, especially IL-6 Gene level of THP-1 cells caused by CpG-c sitimulation.

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