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ABSTRACT: Combination of anlotinib and Tislelizumab for lung adenocarcinoma: effects on metabolic and flora microenvironment and exploration of prognosis-related biomarkers

PROVIDER: PRJNA1010469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25782570_1.fastq.gz	Fastqsanger.gz
	SRR25782570_2.fastq.gz	Fastqsanger.gz
	SRR25782571_1.fastq.gz	Fastqsanger.gz
	SRR25782571_2.fastq.gz	Fastqsanger.gz
	SRR25782572_1.fastq.gz	Fastqsanger.gz

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Role of Anlotinib-induced CCL2 decrease in anti-angiogensis and response prediction for Non-Small Cell Lung Cancer therapy

Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.

2018-11-30 | E-MTAB-5997 | biostudies-arrayexpress

Enhancing Tumor Targeting of Antitumor Drugs through Anlotinib-Mediated Modulation of Extracellular Matrix and RhoA/ROCK Signaling Pathway

Project description:In this study, our research focused on investigating the impact of Anlotinib in enhancing the tumor targeting of antitumor drugs in vivo. Through RNA-sequencing and Label-free quantitative proteomics analysis, we discovered that Anlotinib effectively regulated the expression of extracellular matrix (ECM) genes and proteins, leading to a significant reduction in ECM stiffness. Our bioinformatic analysis indicated a potential positive relationship between the ECM pathways and gefitinib resistance, poor PD-1 treatment outcomes, as well as unfavorable prognosis in lung cancer patients following chemotherapy. To evaluate the efficacy of Anlotinib, we administered it in combination with anti-PD-1/PD-L1 agents, chemotherapeutic drugs, and gefitinib, and visualized their distribution using fluorescent labeling in various tumor types. Notably, our results demonstrated that Anlotinib substantially improved the drug targeting process by prolonging the retention time of antitumor drugs at the tumor site. Moreover, the combination therapy induced a notable loosening of the tumor tissue structure compared to the control group. This reduction in stiffness was further associated with decreased interstitial fluid pressures and tumor solid pressure. Additionally, we observed that Anlotinib effectively suppressed the RhoA/ROCK signaling pathway, inhibiting the formation of stress fibers. These findings strongly suggest that Anlotinib enhances the distribution and retention of antitumor drugs in tumors by modulating ECM expression and physical properties through the RhoA/ROCK signaling pathway. These valuable insights contribute to the development of combination therapies aimed at improving tumor targeting in cancer treatment.

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Project description:Combination of anlotinib and Tislelizumab for lung adenocarcinoma: effects on Transcriptome

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An inflammatory single-cell RNA sequencing signature driven by metabolic stress in a new mouse model of heart failure with preserved ejection fraction and its reversion by the SGLT2 inhibitor dapagliflozin [scRNA-Seq cd45+]

Project description:Heart failure with preserved ejection fraction (HFpEF) is a public health problem with increasing incidence and prevalence. Different phenotypes have been identified based on related risk factors, cardiac structural alterations, biomarkers and prognosis. Among these, the one with the worst prognosis is characterized by metabolic dysfunction . This clinical phenotype exhibits high levels of biomarkers related to dysregulated metabolism and TNF-a–mediated inflammation, thus underlying its close association with metabolic dysfunction and inflammation. The aim of our work is to better comprehend the involvement of the immune cells in the pathogenesis of metabolic HFpEF and to determine whether treating metabolic dysfunction with SGLT2i could ameliorate HFpEF by decreasing myocardial inflammation.

2023-12-22 | GSE208425 | GEO

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Project description:Heart failure with preserved ejection fraction (HFpEF) is a public health problem with increasing incidence and prevalence. Different phenotypes have been identified based on related risk factors, cardiac structural alterations, biomarkers and prognosis. Among these, the one with the worst prognosis is characterized by metabolic dysfunction . This clinical phenotype exhibits high levels of biomarkers related to dysregulated metabolism and TNF-a–mediated inflammation, thus underlying its close association with metabolic dysfunction and inflammation. The aim of our work is to better comprehend the involvement of the immune cells in the pathogenesis of metabolic HFpEF and the effect of local inflammatory activation on cardiomyocyte function.

2023-12-22 | GSE209548 | GEO

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Project description:Further to our previous study (E-MTAB-5997), here we performed transcriptome profiling on Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975, and would like to understand the effects of Anlotinib on Anlotinib-resistant NCI-H1975 cell, compare the different transcriptome profiling on NCI-H1975 cells and Anlotinib-resistant NCI-H1975 cells, sought to find the biomarker for explaining Anlotinib resistance.

2019-07-01 | E-MTAB-7068 | biostudies-arrayexpress

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Project description:Primary retroperitoneal liposarcoma (RLPS) is a rare heterogeneous tumor occurring within retroperitoneal space, and its overall survival did not improve much in the past few decades. Based on a small-sample clinical practice at our center, patients with RLPS can greatly benefit from combination of anlotinib and eribulin. In this study, we investigated combinational effect of anlotinib and eribulin on RLPS. Through transcriptome analysis, we uncovered and validated that synergistic effect mainly induced by endoplasmic reticulum stress (ERS) pathway both in vitro and in vivo.

2024-08-01 | GSE261076 | GEO

Spatially Resolved Multi-Omics Single-Cell Analyses Inform Mechanisms of Immune Dysfunction in Pancreatic Cancer

Project description:As pancreatic ductal adenocarcinoma (PDAC) continues to be recalcitrant to therapeutic interventions including poor response to immunotherapy, albeit effective in other solid malignancies, a more nuanced understanding of the immune microenvironment in PDAC is urgently needed. Using a spatially-resolved multimodal single cell approach we unveil a detailed view of the immune micromilieu in PDAC with specific emphasis on the correlation of immune subtypes with patient prognosis. We substantiate the exhausted phenotype of CD8 T cells and immunosuppressive features of myeloid cells, and highlight immune subpopulations with potentially underappreciated roles in PDAC that diverge from immune populations within adjacent normal areas, particularly CD4 T cell subsets presenting immunosuppressive phenotypes with varying modes of exhaustion. We reveal striking differences between immune phenotypes in PDAC and lung adenocarcinoma, which explain their differential responsiveness to current immunotherapies, providing a comprehensive resource for functional studies and the exploration of therapeutically actionable targets in PDAC.

2023-07-20 | GSE205049 | GEO

Gene expression after human PANC-1 cells treated with anlotinib by a microarray profiling (Affymetrix)

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