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LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [lnc RNA-Seq]

ABSTRACT: LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [lnc RNA-Seq]

PROVIDER: PRJNA1027080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26357702_1.fastq.gz	Fastqsanger.gz
	SRR26357702_2.fastq.gz	Fastqsanger.gz
	SRR26357703_1.fastq.gz	Fastqsanger.gz
	SRR26357703_2.fastq.gz	Fastqsanger.gz
	SRR26357704_1.fastq.gz	Fastqsanger.gz

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LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [lnc RNA-Seq]

Project description:Accumulated data demonstrate that cancer stem-like cell is a key barrier for therapeutic resistance and metastasis in various cancers, including breast cancer, yet the underlying mechanisms are still elusive. Through a genome-wide lncRNA expression profiling, we identified that LINC00115 is robustly upregulated in chemoresistant breast cancer stem-like cells (BCSCs). LINC00115 functions as a scaffold lncRNA to link SETDB1 and PLK3, leading to enhanced SETDB1 methylation of PLK3 at both K106 and K200 in drug-resistant BCSC. PLK3 methylation decreases PLK3 phosphorylation of HIF1α and thereby increases HIF1α stability. HIF1α, in turn, upregulates ALKBH5 to reduce m6A modification of LINC00115, resulting in attenuated degradation of YTHDF2-dependent m6A-modified RNA and enhanced LINC00115 stability. Thus, this positive feedback loop provokes BCSC phenotypes and enhances chemoresistance and metastasis in triple-negative breast cancer. Our findings uncover LINC00115 as a critical regulator of BCSC and highlight potential therapeutic strategies for therapeutic resistance and metastasis in breast cancer.

2024-03-27 | GSE245143 | GEO

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [RNA-Seq]

2024-03-27 | GSE245144 | GEO

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling

Project description:LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling

| PRJNA1027074 | ENA

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [RNA-Seq]

Project description:LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling [RNA-Seq]

| PRJNA1027079 | ENA

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling

Project description: Not available

| S-EPMC10958889 | biostudies-literature

LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-03-27 | GSE245145 | GEO

CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

Project description:Purpose: The purpose is to systemically identify RNA expression changes after lnc-Dpf3 knockdown in CCR7-stimulated mDCs Methods: We profiled RNA seq in mDCs transfected with si-Lnc-Dpf3 or si-NC and stimulated with or without CCR7 ligand CCL19 and CCL21. Results: CCR7 stimulation induced profound RNA expression changes in mDCs, and a set of genes were differentially expressed in lnc-Dpf3-knockdown DC

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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

Project description:CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

Project description:CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

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lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

2018-11-07 | PXD011577 | Pride

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