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Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549 and H1299]

ABSTRACT: Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549 and H1299]

PROVIDER: PRJNA1212023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32033541.fastq.gz	Fastqsanger.gz
	SRR32033542.fastq.gz	Fastqsanger.gz
	SRR32033543.fastq.gz	Fastqsanger.gz
	SRR32033544.fastq.gz	Fastqsanger.gz
	SRR32033545.fastq.gz	Fastqsanger.gz

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Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549 and H1299]

Project description:Chronic psychological stress is closely linked to malignant disorders, with novel modulators potentially mitigating tumor progression by regulating interactions between neoplastic cells and immune cells. This study identified lncRNA HIF1A-AS3 as a key driver of stress-induced lung cancer progression. Chronic stress models in mice with implanted lung cancer cells revealed significant upregulation of HIF1A-AS3 in stressed groups and human lung cancer tissues. Functional studies showed HIF1A-AS3 promotes cancer cell proliferation and invasion by activating HIF-1ɑ translation through interaction with YBX1, forming a positive feedback loop where HIF-1ɑ enhances HIF1A-AS3 transcription. Additionally, HIF1A-AS3 drove macrophage M2 polarization and reduced phagocytosis under hypoxia. Targeting the HIF1A-AS3/HIF-1ɑ loop effectively counteracted stress-induced lung cancer progression in vivo, highlighting its potential as a diagnostic and therapeutic target for stress-exacerbated lung cancer.

2025-03-26 | GSE287281 | GEO

Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation

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Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549_xenograft]

2025-03-26 | GSE287282 | GEO

Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation

Project description:Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation

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Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549_xenograft]

Project description:Chronic stress stimulated HIF-AS3/HIF-1α loop in neoplastic cells and promoted lung cancer progression through macrophage inactivation [A549_xenograft]

| PRJNA1212021 | ENA

HOXB-AS3 expressions promote cell proliferation

Project description:We knock down HOXB-AS3 with shRNA in OCI/AML3 cell line to investigate the downstream pathways of HOXB-AS3 in the cell proliferation.

2019-07-16 | GSE114823 | GEO

The long non-coding RNA HOXB-AS3 regulates ribosomal RNA transcription in NPM1-mutated acute myeloid leukemia

Project description:In this work we dissect the functional role of the HOXB-AS3 long non coding RNA in patients with NPM1-mutated (NPM1mut) acute myeloid leukemia (AML). We show that HOXB-AS3 regulates the proliferative capacity of NPM1mut AML blasts in vitro and in vivo. HOXB-AS3 was found to interact with the ErbB3-binding protein 1 (EBP1) and guide EBP1 to the ribosomal DNA locus. Via this mechanism HOXB-AS3 regulates ribosomal RNA transcription and de novo protein synthesis. We propose that in the context of NPM1 mutations, HOXB-AS3 overexpression acts as a compensatory mechanism, which allows adequate protein production in leukemic blasts.

2019-10-16 | PXD015520 | Pride

A novel long non-coding RNA HOXC-AS3 mediates tumorigenesis of gastric cancer by binding to YBX1

Project description:Recently, increasing evidence shows that long noncoding RNAs (lncRNAs) play a significant role in human tumorigenesis. However, the function of lncRNAs in human gastric cancer remains largely unknown. By using publicly available expression profiling data from gastric cancer and integrating bioinformatics analyses, we screen and identify a novel lncRNA, HOXC-AS3. HOXC-AS3 is significantly increased in gastric cancer tissues and is correlated with clinical outcomes of gastric cancer. In addition, HOXC-AS3 regulates cell proliferation and migration both in vitro and in vivo. RNA-seq analysis reveals that HOXC-AS3 knockdown preferentially affects genes that are linked to proliferation and migration. Mechanistically, we find that HOXC-AS3 is obviously activated by gain of H3K4me3 and H3K27ac, both in cells and in tissues. RNA pull down-mass spectrometry analysis identifies that YBX1 interacts with HOXC-AS3, and RNA-seq analysis finds a marked overlap in genes differentially expressed after YBX1 knockdown and those transcriptionally regulated by HOXC-AS3, suggesting that YBX1 participates in HOXC-AS3-mediated gene transcriptional regulation in the tumorigenesis of gastric cancer.Together, our data demonstrate that abnormal histone modification-activated HOXC-AS3 may play important roles in gastric cancer oncogenesis and may serve as a target for gastric cancer diagnosis and therapy.

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Acinetobacter sp. AS3

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Gene Expression profiles of colon from Hif-1α+/+, Hif-1αLSL/LSL

Project description:To investigate the detailed molecular mechanisms for the regulatory role of HIF-1α in colon, microarray gene expression analysis was performed on colon RNA isolated from 6- to 8-week-old Hif-1α+/+, Hif-1αLSL/LSL mice. Background & Aims: The progression and growth of solid tumors leads to a state where tumors outgrow their capacity for efficient oxygenation and nutrient uptake and an increase in tumor hypoxia. Tumor hypoxic response is mediated by hypoxia-inducible factor (HIF)-1a and HIF-2a. These transcription factors regulate a battery of genes that are critical for tumor oxygenation, tumor metabolism, and cell proliferation and survival. Therefore, inhibitors of HIF have been sought for as anti-neoplastic agents in several different kinds of cancers. Interestingly, in ischemic and inflammatory diseases of the intestine, activation of HIF-1a is beneficial, and can reduce intestinal inflammation. The efficacy of pharmacological agents that chronically activate HIF-1a are decreased due to the tumorigenic potential of HIF. However, recent advance in understanding HIF signaling have identified mechanisms, which could allow for isoform specific activators. Activation of HIF-2a increases colon carcinogenesis and progression in mouse models. However, the role of chronic HIF-1a activation is unclear in the progression in colon cancer. The present data demonstrates that activation of HIF-1a in epithelial cells does not increase colon carcinogens or progression in two mouse models of colon cancer, and provides the proof of principle that HIF-1a activation maybe safe as therapies for inflammatory bowel disease. Global gene expression profiling in colon RNAs isolated from 6- to 8-week-old Hif-1α+/+ (n=5, Shah 019) and Hif-1αLSL/LSL (n=5, Shah 020).

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