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LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (ChiRP-Seq)

ABSTRACT: LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (ChiRP-Seq)

PROVIDER: PRJNA521057 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8534560_1.fastq.gz	Fastqsanger.gz
	SRR8534560_2.fastq.gz	Fastqsanger.gz
	SRR8534561_1.fastq.gz	Fastqsanger.gz
	SRR8534561_2.fastq.gz	Fastqsanger.gz
	SRR8534562_1.fastq.gz	Fastqsanger.gz

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LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (ChiRP-Seq)

Project description:Hepatocellular carcinoma (HCC) is the most prevalent liver cancer, characterized by a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may well contribute to both of these pathological properties, but the mechanism underlying their self-renewal and maintenance are poorly understood. Here we identified a long noncoding RNA (lncRNA) termed HAND2-AS1 that is highly expressed in liver CSCs. Human HAND2-AS1 is highly conserved to its mouse ortholog lncHand2. HAND2-AS1 is required for the self-renewal maintenance of liver CSCs to initiate HCC development. Mechanically, HAND2-AS1 recruits the INO80 complex onto BMPR1A promoter to trigger its expression, leading to the activation of BMP signaling. Importantly, targeting HAND2-AS1 by antisense oligonucleotides (ASOs) and BMPR1A by siRNAs have synergistic anti-tumor effects on humanized HCC models. Moreover, knockout of lncHand2 or Bmpr1a in mouse hepatocytes impairs BMP signaling and suppresses the initiation of liver cancer. Our findings reveal that HAND2-AS1 promotes the self-renewal of liver CSCs and drives liver oncogenesis, which may be a potential target for HCC therapy.

2019-02-06 | GSE126122 | GEO

LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (RNA microarray)

Project description:Investigation the RNA profiling in Huh7 cells upon knock-out lncRNA HAND2-AS1 or knock-down INO80 via gene expression microarray analysis Hepatocellular carcinoma (HCC) is the most prevalent liver cancer, characterized by a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may well contribute to both of these pathological properties, but the mechanism underlying their self-renewal and maintenance are poorly understood. Here we identified a long noncoding RNA (lncRNA) termed HAND2-AS1 that is highly expressed in liver CSCs. Human HAND2-AS1 is highly conserved to its mouse ortholog lncHand2. HAND2-AS1 is required for the self-renewal maintenance of liver CSCs to initiate HCC development. Mechanically, HAND2-AS1 recruits the INO80 complex onto BMPR1A promoter to trigger its expression, leading to the activation of BMP signaling. Importantly, targeting HAND2-AS1 by antisense oligonucleotides (ASOs) and BMPR1A by siRNAs have synergistic anti-tumor effects on humanized HCC models. Moreover, knockout of lncHand2 or Bmpr1a in mouse hepatocytes impairs BMP signaling and suppresses the initiation of liver cancer. Our findings reveal that HAND2-AS1 promotes the self-renewal of liver CSCs and drives liver oncogenesis, which may be a potential target for HCC therapy.

2019-02-06 | GSE126121 | GEO

LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target

Project description:LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target

| PRJNA521054 | ENA

LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (RNA microarray)

Project description:LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target (RNA microarray)

| PRJNA521056 | ENA

LncRNA HAND2-AS1 controls liver cancer stem cell functions and serves as a potential therapy target

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

2019-02-06 | GSE126123 | GEO

Gene expression profiling of uterine stromal cells isolated from Hand2 floxed and Hand2 ablated mice on day 4 of pregnancy

Project description:Our previous study revealed that the basic helix-loop-helix transcription factor Hand2 is a downstream target of progesterone signaling in mouse uterine stroma at the time of implantation. Further, conditional deletion of Hand2 in mouse uterus leads to implantation failure due to impaired uterine epithelial receptivity. To identify the downstream targets of Hand2 in the uterus, we performed gene expression profling of uterine stromal cells isolated from Hand2-null mice and the corresponding controls on day4 of pregnancy (the time of implantation). The microarray results revealed elevated expression of mRNAs corresponding to several members of the fibroblast growth factor family in uterine stroma of Hand2-ablated mice. These factors act as paracrine mediators of mitogenic effects of estrogen on the epithleium. Thus, Hand2 is a critical regulator of the uteirne stromal-epithelial communication that directs proper steroid regulation conducive for establshment of pregnancy. We performed conditional ablation of Hand2 in the mouse uterus using the PRcre mouse model. As Hand2 expression is restricted to stromal comaprtment, we isolated uterine stromal cells from day4 pregnant mice (n=5 for each genotype), purified total RNA from these cells, pooled these samples and then hybridized to high density affymetrix microarrays. Control vs. KO.

2011-06-03 | E-GEOD-25881 | biostudies-arrayexpress

Expression data from Hand2 mutant mouse embryos

Project description:Acquisition of the lower jaw (mandible) was evolutionarily important for jawed vertebrates. In humans, syndromic craniofacial malformations often accompany jaw anomalies. Hand2 is involved in coordinating the developmental network of mandibles and the oral apparatus through Hand2-downstream genes and is therefore a major determinant of jaw identity. We used microarrays to detail the global programme of gene expression involved in mandible specification and identified distinct classes of up-regulated genes during this process. Wild-type and Hand2 mutant (Hand2 CAT/+; Wnt1-Cre) embryos were collected at Embryonic day (E) 11.5 or E12.5 for RNA extraction and hybridization on Affymetrix microarrays.

2015-12-15 | E-GEOD-75805 | biostudies-arrayexpress

Gene profiling of Hand2 target genes and transcriptional regulation of Hand2 expression in the postnatal myocardium

Project description:In humans, cardiac hypertrophy is the principal risk factor for the development of overt heart failure and sudden cardiac death from lethal arrhythmias. Although aberrant reactivation of fetal² gene programs is intricately linked to maladaptive hypertrophy of postnatal cardiomyocytes, loss of cardiac function and heart failure, the transcription factors driving these gene programs remain ill defined. We report that the basic helix-loop-helix (bHLH) transcription factor dHAND/Hand2 is re-expressed in the mammalian postnatal myocardium in response to stress signaling. Interestingly, mutant mice overexpressing Hand2 in otherwise healthy ventricular myocytes developed a phenotype of pathological hypertrophy. In contrast, conditional gene-targeted Hand2 mice demonstrated a marked resistance to pressure overload-induced hypertrophy, fibrosis, ventricular dysfunction and induction of a fetal gene program. These data suggest a critical role for the Hand2 transcription factor during hypertrophic remodeling and heart failure. To gain more mechanistically insight in the processes underlying heart failure, we here identified Hand2 target genes by microarray gene expression profiling. RNA samples were collected 4 weeks after sham or TAC surgery (to induce pressure overload) of both tamoxifen-treated Hand2f/f (WT) and MCM-Hand2f/f (KO) mice.

2013-11-15 | E-MTAB-1821 | biostudies-arrayexpress

Transcription profile of zebrafish hand2 (hanS6 allele) mutant embryos at 19hpf

Project description:Heart formation requires the fusion of bilateral cardiomyocyte populations as they move toward the embryonic midline. The bHLH transcription factor Hand2 is essential for cardiac fusion; however, the effector genes that execute this function of Hand2 are unknown. Here, we provide the first evidence for a downstream component of the Hand2 pathway that mediates cardiac morphogenesis. Although hand2 is expressed in cardiomyocytes, mosaic analysis demonstrates that hand2 plays a non-autonomous role in regulating cardiomyocyte movement. Gene expression profiles reveal heightened expression of fibronectin 1 (fn1) in hand2 mutant embryos. Reciprocally, overexpression of hand2 leads to decreased Fibronectin levels. Furthermore, reduction of fn1 function enables rescue of cardiac fusion in hand2 mutants: bilateral cardiomyocyte populations merge and exhibit improved tissue architecture, albeit without major changes in apicobasal polarity. Together, our data provide a novel example of a tissue creating a favorable environment for its morphogenesis: the Hand2 pathway establishes an appropriate environment for cardiac fusion through negative modulation of Fn1 levels. Embryos from three independent hand2 mutant (hanS6 allele) heterozyogous crosses were collected. Examination of Tg(myl7:egfp) expression allow sorting of hand2 mutant embryos from their wild-type siblings.

2010-08-03 | E-GEOD-23381 | biostudies-arrayexpress

HAND2 regulates regional chromation modification [HAND2-knockdown_histone_ChIPseq]

Project description:The knockdown of HAND2 affects the regional chromation modification.

2023-03-29 | GSE184058 | GEO